Size and albedo of Kuiper belt object 55636 from a stellar occultation.

The Kuiper belt is a collection of small bodies (Kuiper belt objects, KBOs) that lie beyond the orbit of Neptune and which are believed to have formed contemporaneously with the planets. Their small size and great distance make them difficult to study. KBO 55636 (2002 TX(300)) is a member of the water-ice-rich Haumea KBO collisional family. The Haumea family are among the most highly reflective objects in the Solar System. Dynamical calculations indicate that the collision that created KBO 55636 occurred at least 1 Gyr ago. Here we report observations of a multi-chord stellar occultation by KBO 55636, which occurred on 9 October 2009 ut. We find that it has a mean radius of 143 +/- 5 km (assuming a circular solution). Allowing for possible elliptical shapes, we find a geometric albedo of in the V photometric band, which establishes that KBO 55636 is smaller than previously thought and that, like its parent body, it is highly reflective. The dynamical age implies either that KBO 55636 has an active resurfacing mechanism, or that fresh water-ice in the outer Solar System can persist for gigayear timescales.

The recent expansion of Pluto's atmosphere.

Stellar occultations--the passing of a relatively nearby body in front of a background star--can be used to probe the atmosphere of the closer body with a spatial resolution of a few kilometres (ref. 1). Such observations can yield the scale height, temperature profile, and other information about the structure of the occulting atmosphere. Occultation data acquired for Pluto's atmosphere in 1988 revealed a nearly isothermal atmosphere above a radius of approximately 1,215 km. Below this level, the data could be interpreted as indicating either an extinction layer or the onset of a large thermal gradient, calling into question the fundamental structure of this atmosphere. Another question is to what extent Pluto's atmosphere might be collapsing as it recedes from the Sun (passing perihelion in 1989 in its 248-year orbital period), owing to the extreme sensitivity of the equilibrium surface pressure to the surface temperature. Here we report observations at a variety of visible and infrared wavelengths of an occultation of a star by Pluto in August 2002. These data reveal evidence for extinction in Pluto's atmosphere and show that it has indeed changed, having expanded rather than collapsed, since 1988.

Tissue renin-angiotensin system: a site of drug action?

In this review, we present background material that provides partial support for a tissue renin-angiotensin system (RAS). Evidence for the existence of this system relied in part on the use of drugs, which has entailed using low doses or concentrations of angiotensin-converting enzyme inhibitors, renin inhibitors, and angiotensin antagonists to block the RAS in vascular beds and in isolated arteries or organs. Other evidence for a tissue RAS has depended upon measurements of the components of the system, i.e. enzymes, substrates, and mRNAs for these proteins. All of these components were first believed to be present in the heart and blood vessels; however, it is now known that renin in the circulating blood derived from the kidney is used for the local synthesis of angiotensins. The main emphasis of the review is on the renal RAS because it is believed that the local RAS is most prominent in this organ. The renal RAS is probably involved in the long-rather than short-term regulation of renal vascular resistance and maintenance of normal blood pressure through the regulation of sodium reabsorption.

Kinin-mediated antihypertensive effect of captopril in deoxycorticosterone acetate-salt hypertension.

On the basis of evidence suggesting the activation of the kallikrein-kinin system in steroid-induced hypertension, we considered the possibility that the angiotensin-converting enzyme inhibitor captopril would lower the arterial blood pressure in deoxycorticosterone acetate (DOCA)-salt hypertensive rats through kininase II inhibition. In conscious DOCA-salt hypertensive rats with intact kidneys (n = 6) or uninephrectomized rats (n = 5), the short-term administration of captopril (8 mg/kg IV) decreased mean blood pressure from 141 +/- 3 to 118 +/- 3 mm Hg (P < .05) and from 176 +/- 12 to 158 +/- 15 mm Hg (P < .05), respectively. The maximal effect of captopril was manifested between 40 and 50 minutes after its administration, and blood pressure remained depressed for at least 2 hours. The bradykinin B2 receptor antagonist Hoe 140 (500 micrograms/kg IV) abolished the antihypertensive effect of captopril in the DOCA-salt hypertensive rats, indicating kinin involvement. Losartan, an angiotensin type 1 receptor antagonist, had no effect on blood pressure in another group of DOCA-salt hypertensive rats (n = 9) and did not significantly change the response to captopril. No effect of the angiotensin-converting enzyme inhibitor was seen in normotensive control rats (n = 5), indicating the absence of a nonspecific hypotensive action of the drug. Plasma renin activity was lower in the DOCA-salt hypertensive rats (0.7 +/- 0.2 ng angiotensin I/mL per hour, n = 4) than in normotensive control rats (8.8 +/- 1.7, n = 4). The involvement of kinins in the antihypertensive effect of captopril in DOCA-salt hypertension supports the contention that the kallikrein-kinin system contributes to blood pressure regulation in this hypertension model.

Threshold sodium excretory and renal blood flow effects of angiotensin converting enzyme inhibition.

OBJECTIVE: To probe the potential influence of a high renal tubular level of angiotensin II on sodium reabsorption using angiotensin converting enzyme inhibitors and a non-peptide angiotensin antagonist. METHODS: Systemic arterial blood pressure, renal blood flow (RBF) and electrolyte and urinary excretion were measured in anesthetized uninephrectomized Wistar rats. Captopril (n = 12), ramiprilat (n = 10) or EXP 3174 (n = 9) was infused into the renal artery in graded doses to examine whether the threshold dose that increased RBF was lower than that which increased sodium excretion rate (Na+ excretion rate). RESULTS: Whereas ramiprilat (0.5-4 micrograms/kg/min intra-arterially) and EXP 3174 (0.5-4 micrograms/kg/min intra-arterially) decreased blood pressure in all but the lowest dose of 0.5 micrograms/kg/min, captopril (1-8 micrograms/kg/min intra-arterially) did not change blood pressure except for a slight effect with the two higher doses. These three agents increased RBF to about the same degree, between 6% and 18%, which was relatively large compared with the maximal vasodilator response achievable in the kidney with acetylcholine (30-37%). Captopril given intra-arterially had a more consistent effect on Na+ excretion rate than either ramiprilat or EXP 3174. An increase in Na+ excretion rate occurred with captopril ranging from 44% to 78%, whereas no significant change was obtained with the other drugs. The dose of captopril that increased RBF was the same as that which increased Na+ excretion rate. In those experiments in which ramiprilat resulted in an increase in Na+ excretion rate (five of 10 experiments), the effective dose was the same as that which increased RBF. CONCLUSION: When administered by the intra-arterial route, captopril was more effective in increasing Na+ excretion rate than either ramiprilat or EXP 3174. Although the threshold dose of captopril and ramiprilat required to increase Na+ excretion rate and RBF was similar, suggesting blockade of a common angiotensin II pool, there was not a good correlation between these two effects.

Rat renal papillary release of hypotensive substances in vitro.

Platelet activating factor (PAF) is produced by the rat renal papilla from a neutral lipid, alkylacetylglycerol. Renal release of another neutral lipid, antihypertensive neutral renomedullary lipid, and PAF might account for normalization of blood pressure after unclipping in Goldblatt hypertensive rats. We studied the potential storage and release of hypotensive substances by the rat renal papilla in vitro. Rat kidneys were snap-frozen in liquid N2-cooled freon immediately after removal and the total lipids were extracted from pooled dissected papillae and partially separated by thin layer chromatography on silica gel with a hexane: ether: acetic acid (40:60:1) solvent system. Lipids eluted from four, contiguous silica gel zones were assayed in anesthetized spontaneously hypertensive rats. No hypotensive activity was found in the thin layer chromatography lipid fraction co-migrating with palmitylacetylglycerol or in any other neutral lipid fraction. In contrast, the Krebs medium obtained after 30-min incubation of freshly minced papillary tissue induced dose-related hypotension and bradycardia. The hypotensive activity was equivalent to 48 +/- 9 ng prostaglandin E2 (PGE2)/mg wet papilla. Bradycardia induced by the incubation medium was correlated with decrements in blood pressure. In the same assays, nitroprusside caused tachycardia which was correlated with hypotension, and the bradycardia associated with PGE2-induced hypotension was significantly less than that induced by the incubation medium. The dose-related effects of the incubation medium were dramatically attenuated by indomethacin treatment of the papilla, suggesting that the hypotensive activity is dependent upon papillary cyclooxygenase activity. However, PGI2 elicited hypotension concomitant with tachycardia rather than bradycardia and PGE2 did not mimic the incubation medium-induced bradycardia. Therefore, the effects of the papillary incubation medium may be mediated by other cyclooxygenase metabolites. Production/release of hypotensive material by indomethacin-treated papillary tissue was potentiated by co-incubation with non-hypotensive quantities of PGE2, suggesting a potential role for PGE2 in the renal antihypertensive function. Increasing pressure on the papilla from 6 to 20 mmHg during incubation did not increase release of non-prostanoid hypotensive substance(s). These results suggest that the formation and release of cyclooxygenase metabolites accounts primarily for the hypotensive activity released from rat renal papillae in vitro, and that prostaglandins might play a permissive role in the release of other renomedullary hypotensive substances.

Postunclipping renal blood flow in one-kidney, one-clip hypertensive rats.

Removal of the arterial clip (unclipping) in one-kidney, one-clip (1K, 1C) Goldblatt hypertensive rats causes rapid return of mean arterial pressure (MAP) to normotensive levels. An extracorporeal circulation was established between the renal and jugular veins to evaluate the influence of unclipping on renal blood flow (RBF) in Inactin-anesthetized 1K, 1C rats. MAP in rats with the extracorporeal circulation was 182 +/- 5 mmHg before unclipping or sham operation. MAP decreased to 113 +/- 4 mmHg within 2 h after unclipping compared with 169 +/- 13 mmHg in sham-unclipped rats. RBF increased by 2.8 ml.min-1.g-1 from a basal level of 3.8 +/- 0.3 after unclipping and was maintained approximately 40% above the basal level for 2 h, although renal vascular resistance was 94% greater than in uninephrectomized control rats. Heart rate did not change in either unclipped or sham-operated rats. Indomethacin (7 mg/kg) did not affect unclipping-induced changes in MAP, RBF, or urine output; however heart rate decreased immediately after unclipping and remained approximately 25-35 beats/min below control levels for the 2-h observation period. In rats lacking the extracorporeal circuit, MAP decreased (P less than 0.005) and heart rate increased (P less than 0.05) in response to unclipping. Nevertheless, unclipping-induced tachycardia was significantly less than that caused by nitroprusside infusions causing similar decrements in MAP. The results suggest that the sustained increment in RBF after unclipping in chronic, established 1K, 1C hypertension may be associated with postunclipping hypotension and diuresis, that blockade of prostaglandin synthesis may unmask unclipping-induced bradycardia, and that prostaglandins are not essential for postunclipping changes in renal hemodynamics.

Antagonism of the vasodilator effects of a platelet activating factor precursor in anesthetized spontaneously hypertensive rats.

The hemodynamic effects of platelet activating factor (PAF), PAF antagonists and a precursor of PAF, 1-palmityl-2-acetyl-glycerol (PAG), were examined in pentobarbital-anesthetized spontaneously hypertensive rats to determine whether functionally significant amounts of PAF are produced via the cholinephosphotransferase pathway of PAF synthesis in vivo. Intravenous bolus doses of PAF, PAG and nitroprusside elicited hypotension and active mesenteric vasodilatation. Responses to PAG were slower in onset and longer in duration than those of PAF and nitroprusside. The specific PAF antagonists, CV-3988 and SRI 63-675, attenuated PAG- and PAF-, but not nitroprusside-induced changes in blood pressure and mesenteric flow/resistance. In contrast, captopril, which blocked the effects of angiotensin I, did not influence the hypotension caused by PAG, PAF and nitroprusside. The results suggest that the vasodilator effects of PAG are attributable to PAF produced from this alkylacetylglycerol, and the renin-angiotensin system does not appear to influence the biotransformation of PAG to PAF or the hypotensive action of PAF.

Limited capacity for renal vasodilatation in anesthetized diabetic rats.

Studies were conducted to determine whether reduced renal blood flow (RBF) exhibited by rats with uncontrolled streptozotocin (STZ)-induced diabetes is attributable to diabetes-induced structural changes in the renal vasculature. Vehicle-treated control rats (CR) and rats that were injected with STZ (STZR) after pretreatment with 3-O-methylglucose (3-OMG), an agent that prevents STZ-induced hyperglycemia, were also studied. Basal values of total RBF (ml.min-1.g kidney wt-1, electromagnetic flow probe), systemic arterial pressure (BP, mmHg), and renal vascular resistance (RVR, BP/RBF) in pentobarbital-anesthetized rats during a control period were 5.4 +/- 0.3 (P less than 0.01 vs. CR), 116 +/- 3, and 21.9 +/- 1.0 (P less than 0.01 vs. CR) in STZR (n = 12) and 8.2 +/- 0.4, 121 +/- 2, and 15.3 +/- 1.0 in CR (n = 11), respectively. Basal values of RBF, BP, and RVR in 3-OMG-pretreated STZR were identical to CR. The relative capacity of STZR and CR kidneys for vasodilatation in situ in response to intrarenal arterial infusions of acetylcholine (ACh) and bradykinin (BK) and systemically administered sodium nitroprusside (NP) was evaluated. The capacity of STZR to exhibit active renal vasodilatation in response to intrarenal arterial ACh and BK was significantly less than that of CR (P less than 0.01). The minimum level to which RVR was suppressed after 50 micrograms NP/kg iv was higher in STZR than in either CR or 3-OMG-pretreated STZR (14.8 +/- 1.5 vs. 9.0 +/- 0.7 and 9.3 +/- 1.5 mmHg.ml-1.min.g kidney wt, respectively; P less than 0.05). This dose of NP exerted effective functional antagonism of renal vasoconstriction induced by exogenous norepinephrine and angiotensin II. These in vivo studies suggest that the elevated RVR in STZR might be attributable in part to structural changes in the renal vasculature that are associated with the diabetic state and limit the capacity for renal vasodilatation. However, there was no difference in pressure-flow relationships between the two groups in maximally dilated isolated kidneys perfused with Krebs buffer containing 5% albumin, and the RBF deficit in STZR kidneys was corrected by perfusion with blood from CR. Thus the decreased RBF exhibited by STRZ in vivo cannot be attributed solely to renal vascular structural changes associated with diabetes. These findings suggest that undefined humoral factors or abnormal interaction of formed blood elements with vessel walls may account for elevated RVR in STZR.

Hypotensive and renal vasodilator effects of carbocyclic adenosine (aristeromycin) in anesthetized spontaneously hypertensive rats.

Systemic arterial pressure and renal blood flow were measured in pentobarbital-anesthetized spontaneously hypertensive rats to assess the influence and mechanism of action of metabolically stable adenosine analogs on renal hemodynamics. (-)-Aristeromycin (carbocyclic adenosine; CA), a model carbocyclic nucleoside, was characterized with respect to adenosine receptor pharmacology by comparison to the effects elicited by the prototypic adenosine analogs 5'-N-ethylcarboxamide adenosine (NECA; an adenosine A1 and A2 receptor agonist) and N6-cyclohexyl adenosine (an adenosine A1 agonist). Intravenous bolus injections of CA and NECA caused dose-dependent hypotension and renal vasodilatation. Although CA and NECA were equally efficacious hypotensive agents, NECA was approximately 100-fold more potent than CA. CA was a more efficacious renal vasodilator than NECA. In contrast, at doses which had minimal effects on systemic arterial pressure, N6-cyclohexyl adenosine decreased renal blood flow. The hypotensive and renovascular effects of the adenosine analogs but not those of a control vasodilator, methacholine, were attenuated by i.v. administration of the xanthines aminophylline and 8-phenyltheophylline; thus, the effects of the nucleosides on renal blood flow in vivo appear to be attributable in part to activation of adenosine receptors. The profile of cardiovascular effects caused by CA suggests that this agent acts primarily as an adenosine A2 receptor agonist.

Reduced prostaglandin synthesis by renal and aortic tissues from adult rats fed essential fatty acid-deficient diet after food deprivation.

Studies were conducted to determine the efficacy of a dietary technique for reducing prostaglandin (PG) synthesis in adult rats. Rats weighing 280-318 g were fed either essential fatty acid (EFA)-deficient or EFA-adequate diets for 10-17 days after a period of food deprivation. Synthesis of renal papillary PGE2 and aortic PGI2 from endogenous precursor in vitro were estimated by liquid chromatographic and bioassay/radioimmunoassay techniques, respectively, as indices of the capacity of the technique to induce EFA deficiency. PGE synthesis and PGI2 synthesis by isolated tissues from rats fed the EFA-deficient diet were significantly decreased (ca. 50%) relative to control rats fed an EFA-adequate diet. Body and renal papillary weights were not significantly altered by the EFA-deficient diet.

Enhanced renal vasoconstriction in rats fed essential fatty acid-deficient diet.

The effects of angiotensin II (ANG II) and norepinephrine (NE) on total renal blood flow (RBF) were studied in rats fed an essential fatty acid (EFA)-deficient diet. EFA deficiency was employed, as an alternative to the use of cyclooxygenase inhibitors, to investigate the influence of arachidonic acid metabolites on rat RBF. Intrarenal arterial (ira) bolus doses of ANG II (2-16 ng) and NE (25-100 ng) elicited significantly greater decrements in RBF and increments in renal vascular resistance in anesthetized Sprague-Dawley rats fed EFA-deficient diets than in control rats, which were fed EFA-adequate diets. Indomethacin (5 mg/kg iv) enhanced the vasoconstrictor responses to ANG II and NE in rats fed the EFA-adequate diet but not in rats fed the EFA-deficient diet. In rats fed regular laboratory chow the renal vasoconstrictor response to ANG II was potentiated after the administration of either indomethacin or naproxen (5 mg/kg iv). Methacholine and prostaglandins E2 and I2 caused dose-related renal vasodilatation when injected (ira) over the dose range of 10-40 ng in rats fed either the EFA-deficient or -adequate diets. The increased responsiveness of the renal vascular bed to ANG II and NE in rats fed EFA-deficient diets was not attributable to reduced vasodilator efficacy. Collectively, these results suggest that the net effect of endoperoxide products of arachidonic acid metabolism attenuates the vasoconstrictor influences of exogenous ANG II and NE in the intact rat kidney.

Alpha-adrenergic stimulation of prostaglandin release from rabbit iris-ciliary body in vitro.

Because previous studies have suggested that ocular effects of adrenergic agonists are in part attributable to arachidonate metabolites, the effect of phenylephrine on synthesis and release of arachidonic acid (AA) and prostaglandins from isolated rabbit iris-ciliary body (ICB) slices was examined. ICB concentrated and incorporated exogenous 14C-AA into tissue phospholipid and neutral lipid stores. During the period of 14C-AA labeling of tissue lipids, a portion of AA was converted to prostaglandins (PGs), as determined by thin-layer chromatography in two solvent systems and by prevention of PG synthesis by indomethacin. PGs E2 and F2 alpha were the major PGs synthesized. PGD2, thromboxane B2, and 6-keto-PGF 1 alpha were also synthesized by ICB. Phenylephrine enhanced PGE2 and PGF2 alpha synthesis and release from superfused 14C-AA-labeled ICB. PGE2 was the major PG released upon stimulation by phenylephrine. Phenoxybenzamine, an alpha-adrenergic receptor antagonists, and indomethacin prevented phenylephrine-induced PG release. The phenylephrine-induced PG release thus represented newly synthesized PG and was a result of the alpha-adrenergic activity of phenylephrine. Phenoxybenzamine treatment did not inhibit enzymes involved in PG synthesis, inasmuch as bradykinin was capable of markedly stimulating PG release from IBC treated with phenoxybenzamine. Esterification of 14C-AA into a lipid tentatively identified as 1,2-diacylglycerol was also demonstrated. The presence of this glyceride suggests that ICB exhibits phosphatidylinositol turnover and that phospholipase C and diacylglycerol lipase activities might be involved in supplying AA for ocular PG synthesis upon alpha-adrenergic stimulation.

Synthesis and biological evaluation of 9,11-azo-13-oxa-15-hydroxyprostanoic acid, a potent inhibitor of platelet aggregation.

The synthesis of a prostaglandin endoperoxide analogue, 9,11-azo-13-oxa-15-hydroxyprostanoic acid (AOHP), is described. AOHP was found to block effectively both the thromboxane synthetase and the PGH2/TxA2 receptors in human platelets. It inhibits the platelet aggregation induced by arachidonic acid, 9.11-methanoepoxy-PGH2, PGH2, and TxA2 but does not affect the ADP-induced aggregation in aspirinated platelet-rich plasma. Some of the intermediates for the synthesis of AOHP also are effective in inhibiting platelet aggregation.

Identification of 15-keto-9, 11-peroxidoprosta-5, 13- dienoic acid as a hematin-catalyzed decomposition product of 15-hydroperoxy-9, 11-peroxidoprosta-5, 13-dienoic acid.

A labile prostaglandin was isolated as one of the products generated from [1-14C] eicosatetraenoic acid incubated with sheep vesicular gland microsomes. The eicosatetraenoic acid metabolite amounted to ca. 16% of the total radiolabeled products. Formation of this new prostaglandin was prevented when heat-denatured microsomes were employed or when incubation mixtures were supplemented with indomethacin or phenol. However, incubation of prostaglandin G2 (PGG2) with hematin in the presence or absence of catalytically active or heat-inactivated microsomes led to production of approximately the same quantity of the new prostaglandin. These results indicated that the new prostaglandin can be formed nonenzymically. The new prostaglandin was conclusively identified by gas liquid chromatography-mass spectrometry analysis as 15-keto-9,11-peroxidoprosta-5,13-dienoic acid (15-keto-PGG2) after chemical conversion to known prostaglandins. The effects of 15-keto-PGG2 and PGG2 were similar on canine lateral saphenous vein; both promoted contraction followed by prolonged relaxation, but 15-keto-PGG2 appeared to be 1/50 as potent as PGG2.

Effects of essential fatty acid deficiency on prostaglandin synthesis and fatty acid composition in rat renal medulla.

Studies are reported on the capacity of isolated rat renal papilla (inner medulla) to synthesize and release prostaglandin (PG) E from endogenous and exogenous precursor(s) during development of an essential fatty acid (EFA) deficiency in the rat. Weanling (21-day-old) male Sprague-Dawley rats were fed a fat-free diet supplemented with either 5% hydrogenated coconut oil (HCO) or 5% safflower oil (SO). At approximately 3, 6 and 7 weeks (6. 9 and 10 weeks of age), groups of animals fed each diet were killed for studies of PGE synthesis in the renal papillae. Differences in the fatty acid composition of the papillae lipids of the animals of each group were also determined. The in vitro production of PGE from endogenous precursor(s) was significantly reduced in the papillae from the 6-week-old rats fed the HCO diet compared to the control (SO) rats, and appeared to be near maximally depressed in the 10-week-old animals compared to that of animals fed an EFA deficient diet for over a year in an accessory experiment. Analyses of the fatty acids of the papillae lipids of the HCO groups showed that the levels of 18:2 and 20:4 were markedly reduced, and those of 16:1, 18:1 and 20:3 were elevated compared to the controls even in the 6-week-old animals, typical of an EFA deficiency. The papillae lipids of the animals fed the HCO diet were also depleted of their stores of 22:4 omega 6. A fatty acid believed to be derived by chain elongation of 20:3 omega 9, 22:3, was found in large concentrations in the papillae triglycerides of the EFA deficient rats. Incubations of exogenous arachidonic acid (20:4) in homogenates and tissue slices of the papillae of the HCO dietary groups showed that the PG synthetase was not impaired by an EFA deficiency. The rate of PGE synthesis in the papillae of the EFA deficient animals was generally enhanced when exogenous 20:4 was added, indicating that the concentration of available precursor(s) is a primary factor in the control of PGE synthesis in the papilla of the rat.

The surface of Mars: the view from the viking 2 lander.

Viking 2 lander began imaging the surface of Mars at Utopia Planitia on 3 September 1976. The surface is a boulder-strewn reddish desert cut by troughs that probably form a polygonal network. A plateau can be seen to the east of the spacecraft, which for the most probable lander location is approximately the direction of a tongue of ejecta from the crater Mie. Boulders at the lander 2 site are generally more vesicular than those near lander i. Fines at both lander sites appear to be very fine-grained and to be bound in a duricrust. The pinkish color of the sky, similar to that observed at the lander I site, indicates suspension of surface material. However, the atmospheric optical depth is less than that at the lander I site. After dissipation of a cloud of dust stirred during landing, no changes other than those stemming from sampling activities have been detected in the landscape. No signs of large organisms are apparent at either landing site.

Alteration of vein cyclic 3':5' nucleotide concentrations during changes in contractility.

The relative changes in vascular tissue levels of cyclic 3':5'-guanosine monophosphate (cGMP) and cyclic 3':5'-adenosine monophosphate (cAMP) were determined in bovine and canine vein strips that were quickfrozen during changes in contractility elicited by prostaglandins (PG) or isoproterenol. Prostaglandin F(2alpha)-induced venoconstriction was associated with increased vascular tissue levels of cGMP and increased ratios of cGMP to cAMP concentrations, but no consistent qualitative change in cAMP levels. In contrast, vein cAMP concentrations were increased during administration of the vasodilators PGE(2) and isoproterenol. The results suggest possible opposing roles for the two cyclic nucleotides in vasomotion.