Holocene ice marginal fluctuations of the Qassimiut lobe in South Greenland.

Knowledge about the Holocene evolution of the Greenland ice sheet (GrIS) is important to put the recent observations of ice loss into a longer-term perspective. In this study, we use six new threshold lake records supplemented with two existing lake records to reconstruct the Holocene ice marginal fluctuations of the Qassimiut lobe (QL) - one of the most dynamic parts of the GrIS in South Greenland. Times when the ice margin was close to present extent are characterized by clastic input from the glacier meltwater, whereas periods when the ice margin was behind its present day extent comprise organic-rich sediments. We find that the overall pattern suggests that the central part of the ice lobe in low-lying areas experienced the most prolonged ice retreat from ~9-0.4 cal. ka BP, whereas the more distal parts of the ice lobe at higher elevation re-advanced and remained close to the present extent during the Neoglacial between ~4.4 and 1.8 cal. ka BP. These results demonstrate that the QL was primarily driven by Holocene climate changes, but also emphasises the role of local topography on the ice marginal fluctuations.

Role of cell contractions in cAMP-induced cardiomyocyte atrial natriuretic peptide release.

Incubation of spontaneously beating ventricular cardiomyocytes from neonatal rats with prostaglandin E(2) (0.1 microM) or forskolin (0.1 microM) simultaneously increased the rate of cellular contraction and atrial natriuretic peptide (ANP) secretion. Both responses were maximal within 10-20 min of application and were accompanied by three- to fourfold increases in cAMP formation. By contrast, a higher regimen of forskolin (10 microM) promoted a 20- to 30-fold increase in basal cAMP production, which was accompanied by the abolition of contractile activity and ANP release. Low regimens of forskolin (0.1 microM) doubled the occurrence of cytosolic Ca(2+) transients associated with monolayer contraction, whereas higher regimens of forskolin (10 microM) completely suppressed Ca(2+) transients. Moreover, in quiescent cultures that were pretreated with ryanodine, tetrodotoxin, nifedipine, or butanedione monoxime, prostaglandin E(2) (0.1 microM) and forskolin (0.1 microM) failed to elicit significant ANP secretion, suggesting that cAMP-elevating agents promote ANP secretion to a great extent via an increase in cellular contraction frequency in ventricular cardiomyocytes.

Smooth muscle energetic in the pig coronary artery during a calcium-dependent and a calcium-independent isometric contraction.

Heat production by resting smooth muscle, was measured with a heat-flux micro calorimeter on cut-open segments of pig coronary artery superfused at 30 degrees C, was 0.93+/-0.06 (n=16) mW/g wet weight. Time courses of the increases in isometric tension and heat production with respect to basal during sustained supra maximal acetylcholine stimulation were qualitatively similar: initial peak tapering down to a supra basal plateau. Mean tension-associated heat production over 1 h was 0.16 J/g. During sustained exposure to phorbol 12,13-dibutyrate, supra basal tension and--with a 5-10 min initial delay--supra basal heat progressively increased to a plateau in about 40 min. Mean tension-associated heat production over 1 h was only 0.02 J/g with normal extracellular and intracellular mobilizable Ca2+ pools, and it was further reduced to 0.01 J/g with depleted Ca2+ pools. These results show that the maintenance--if not necessarily the building up--of tension under phorbol 12,13-dibutyrate does not entail any large dissipation of energy and is not dependent on the presence of normal Ca2+ pools.

Role of prostaglandin-mediated cyclic AMP formation in protein kinase C-dependent secretion of atrial natriuretic peptide in rat cardiomyocytes.

The role of endogenous prostaglandin production in phorbol diester-induced myocardial atrial natriuretic peptide (ANP) secretion was investigated in cultured spontaneously beating ventricular rat cardiomyocytes. Incubation of cells with 4 beta-phorbol 12-myristate 13-acetate (PMA; 0.1 microM) led to a rapid response in ANP release, a response accompanied by increases in cellular prostacyclin (PGI2) production, cyclic AMP (cAMP) formation and spontaneous contraction frequency. Although PMA-induced ANP secretion exhibited the pharmacological profile of a protein kinase C (PKC)-mediated event, the response was abolished in the presence of the cyclo-oxygenase inhibitors indomethacin (10 microM) and diclofenac (1 microM), indicating that endogenous prostaglandin production is responsible for PMA-induced ANP secretion in this system. Confirming this, PMA-induced ANP secretion was strongly correlated with endogenous formation of 6-oxo-prostaglandin F1 alpha (r = 0.93, P < 0.0005, n = 11), and exogenously applied PGI2, prostaglandin E2 (PGE2) or prostaglandin F2 alpha (PGF2 alpha) elicited simultaneous increases in cAMP formation, contraction frequency and ANP secretion in these cells. Furthermore, PMA-induced cAMP formation was abolished in the presence of either diclofenac or indomethacin, whereas the cAMP-elevating agent forskolin (0.1 microM) mimicked the secretory and chronotropic effect of PMA in these cells. A role for cAMP in PMA-induced ANP secretion was also apparent insofar as PMA-induced ANP release was substantially decreased in the presence of the Rp-diastereomer of 3',5'-cyclic adenosine monophosphorothioate (Rp-cAMPS; 10 microM), whereas the cAMP-mimetic agent dibutyryl cAMP (10 microM) provoked a rapid increase in ANP secretion in this system. Finally, the Ca(2+)-channel antagonist nifedipine (0.1 microM) severely decreased PGI2-, PGE2- and PMA-induced ANP secretion without affecting PGF2 alpha-induced peptide release, suggesting that PGI2 and/or PGE2, but not PGF2 alpha, are the prostanoids involved in PMA-induced ANP release. Taken together, these results suggest that PKC activation induces ANP secretion in spontaneously beating rat ventricular cardiomyocytes via an autocrine pathway involving increased PGI2 and/or PGE2 formation, a response leading to the activation of a myocardial adenylate cyclase and, subsequently, to that of a nifedipine-sensitive Ca2+ channel.

Protein kinase C-dependent prostaglandin production mediates angiotensin II-induced atrial-natriuretic peptide release.

The respective roles of protein kinase C (PKC) and endogenous prostaglandin formation in angiotensin II (Ang II)-induced myocardial secretion of atrial natriuretic peptide (ANP) was studied in cultured, spontaneously beating, neonatal-rat cardiomyocytes. Incubation of cardiomyocytes with 0.1 microM Ang II led to a rapid but transient increase in particulate-bound PKC activity, a response accompanied by marked increases in cellular 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) generation and ANP secretion. A role for PKC in Ang II-induced 6-oxo-PGF1 alpha formation and ANP secretion was apparent, insofar as both responses were suppressed in the presence of the PKC inhibitors staurosporine (1 microM) and CGP 41251 (1 microM), as well as in cells in which PKC had been previously down-regulated by pretreatment with phorbol diester. Furthermore, Ang II-induced 6-oxo-PGF1 alpha production was found to be strongly correlated with Ang II-induced ANP release (r = 0.87, P < 0.001, n = 6), indicating a role for prostacyclin (PGI2) in Ang II-induced ANP secretion in these cells. This hypothesis was confirmed by finding that both Ang II-induced 6-oxo-PGF1 alpha production and ANP release were abolished in the presence of the respective phospholipase A2 and cyclo-oxygenase inhibitors quinacrine (10 microM) and indomethacin (10 microM), whereas exogenously applied PGI2 (1 microM) and prostaglandin E2 (0.1 microM) mimicked Ang II-induced ANP secretion in this system. Taken together, these results suggest that Ang II induces ANP secretion in spontaneously beating rat cardiomyocytes via a PKC-dependent autocrine pathway involving a cyclo-oxygenase product and a yet-to-be-identified myocardial prostanoid receptor.

Calcium influx in platelet activating factor-induced atrial natriuretic peptide release in rat cardiomyocytes.

Atrial natriuretic peptide (ANP) is released from the myocardium after the activation of protein kinase C and/or ischemia, events that are associated with an increase in platelet activating factor (PAF) production in this tissue. In this study we demonstrate that PAF, but not lyso-PAF, induces a concentration-dependent increase in ANP secretion in spontaneously beating neonatal rat cardiomyocytes, a response associated with increases in cellular adenosine 3',5'-cyclic monophosphate (cAMP) formation, calcium influx, and the mobilization of calcium from intracellular stores. cAMP formation and calcium influx appear to play major roles in PAF-induced ANP secretion in this system, insofar as PAF-induced ANP release was substantially reduced in the presence of the (R)-p-diastereoisomer of adenosine 3',5'-cyclic monophosphorothioate (10 microM), whereas both PAF-induced calcium influx and ANP secretion were abolished in the presence of the calcium channel antagonist nifedipine (0.1 microM). Consistent with these results, N6-2'-O-dibutyryl cAMP (DBcAMP, 10 microM) and/or forskolin (0.1 microM) simultaneously increased cAMP production, calcium influx, and ANP release in these cells, with both DBcAMP- and forskolin-induced ANP secretion being fully abolished in the presence of 0.1 microM nifedipine. Taken together, these results suggest that PAF, DBcAMP, and forskolin promote ANP secretion in spontaneously beating cardiomyocytes via the activation of a cAMP-dependent, nifedipine-sensitive myocardial calcium channel and that calcium influx is a major requirement for cAMP-induced ANP secretion in this system.

[Ca2+]i and protein kinase C in vasopressin-induced prostacyclin and ANP release in rat cardiomyocytes.

Exposure of cultured, spontaneously beating rat cardiomyocytes to arginine vasopressin (AVP) led to marked increases in the release of prostacyclin (PGI2) and atrial natriuretic peptide (ANP). These responses were accompanied by a rapid, transient rise of cytosolic free Ca2+ concentration ([Ca2+]i) and of membranous protein kinase C (PKC) activity. Ca2+ influx and PKC activity appeared to play important but distinct roles in AVP-induced cellular responses, insofar as only AVP-induced ANP secretion was abolished by the Ca2+ channel antagonist nifedipine, whereas both AVP-induced PGI2 production and ANP release were abolished by the PKC inhibitors staurosporine and CGP-41251. The AVP-induced increase in [Ca2+]i could also be mimicked with the vasopressin (V1-subtype) agonist Octapressin, but not with the V2-agonist 1-desamino-8-D-arginine vasopressin, and was fully abolished by the V1-antagonist [d(CH2)5Tyr(Me)]AVP, but not by d(CH2)5-D-Leu-VAVP (V1-/V2-antagonist). These results indicate that V1-vasopressinergic receptors mediate AVP-induced PGI2 production and ANP secretion in rat cardiomyocytes and that, whereas both Ca2+ influx and PKC activation are required for AVP-induced ANP secretion, AVP-induced PGI2 formation is mainly regulated by PKC.

Angiotensin-II induces changes in the cytosolic sodium concentration in bovine adrenal glomerulosa cells: involvement in the activation of aldosterone biosynthesis.

The homeostasis of cytosolic free calcium ([Ca2+]i) and intracellular free sodium ([Na+]i) are linked in many cell types. We, therefore, studied the effect on [Na+]i of two physiological stimulators of aldosterone synthesis that trigger the calcium messenger system, angiotensin-II (Ang II) and potassium ion (K+), in cultured bovine adrenal glomerulosa cells, using the intracellular fluorescent probe for sodium, sodium benzofuran isophthalate. Ang II induced a concentration-dependent and sustained increase in [Na+]i, from a resting value of 9.2 +/- 3.5 to a maximum of 48.5 +/- 5.5 mM (n = 14). This [Na+]i response was mediated by receptors of the AT1 subtype, because it was abolished by losartan (DuP 753). K+ (15 mM) induced a weaker [Na+]i response, from 5.9 +/- 2.6 to 16.8 +/- 2.5 mM (n = 9). In freshly prepared cells, basal [Na+]i was significantly higher (23.9 +/- 1.8 mM; n = 14; P < 0.01) than in cultured cells. Atrial natriuretic peptide, which is known to affect sodium transport in various cell types, did not alter the [Na+]i response elicited by Ang II. Ethylisopropylamiloride, an inhibitor of Na+/H+ exchange, and dichlorobenzamyl, an inhibitor of Na+/Ca2+ exchange, both inhibited in a concentration-dependent manner the Ang II- and K(+)-induced aldosterone response. Isoosmotic replacement of extracellular Na+ markedly reduced basal aldosterone synthesis. Under these conditions, the concentration-response curve for Ang II-induced aldosterone synthesis was shifted to the right, and its maximum was strikingly diminished. These results show that Ang II and, to a lesser extent, K+ induce significant changes in [Na+]i in bovine glomerulosa cells. These [Na+]i changes probably occur through the Na+/H+ and Na+/Ca2+ exchangers and are likely to play a role in activation of the steroidogenic cascade.

Mechanisms controlling caffeine-induced relaxation of coronary artery of the pig.

1. We studied the effects of caffeine on coronary artery smooth muscle of the pig by measuring changes in isometric tension, cytosolic free Ca(2+) concentration ( [Ca2+]i) and transmembrane potential. 2. In the absence of tone, caffeine induced a concentration-dependent transient contraction of coronary artery strips, followed by sustained relaxation. Simultaneously with the relaxation, caffeine, 25 mM, hyperpolarized the smooth muscle cells by 7.7 +/- 0.9 mV. 3. Caffeine caused a concentration-dependent relaxation of strips precontracted with 10(-5)M acetylcholine (ACH). A supramaximal relaxing concentration of 25 mM caffeine produced an additional transient increase in [Ca2+]i on the Ca2+ plateau of ACh tonic contraction, which was followed by a decrease in [Ca2+]i to a level slightly below the basal concentration. This relaxation was accompanied by a hyperpolarization of 7.3 +/- 0.9 mV. 4. KCI 120 mM (high K+) contracted the strips with a concomitant depolarization of 38.6 +/- 1.6 mV and sustained increase in [Ca2+]i. Caffeine caused a concentration-dependent relaxation of high K+-induced contraction. Caffeine, 25 mM, decreased the Ca2+ plateau to a level that remained above the basal concentration of Ca2+ but did not change the membrane potential. 5. When strips were placed in a Ca(2+)-free medium with EGTA 2mM, and, in addition, ACh was applied successively three times, both intracellular and extracellular mobilizable Ca2+ pools were depleted. In these conditions, phorbol 12,13 dibutyrate (PDBu) 10(-7) M and prostaglandin F 2 alpha (PGF 2 alpha) 10(-5) M contracted the strips. Caffeine (25 mM) inhibited these contractions with no change in [Ca2+]i. 6. Forskolin, 3 x 10 -7M, inhibited ACh induced-contraction but did not affect those induced by PDBu. 7. In conclusion, these results show that caffeine has multiple cellular effects. During caffeine-induced relaxation, [Ca2" Ii, adenosine 3': 5'-cyclic monophosphate (cyclic AMP) content and membrane potential are modified. The findings suggest, however, that these effects are secondary, and that caffeine acts mainly by another unknown mechanism, possibly involving a direct inhibition of the contractile apparatus.

Hemoglobin causes both endothelium-dependent and endothelium-independent contraction of the pig coronary arteries, independently of an inhibition of EDRF effects.

Hemoglobin is widely used as an inhibitor of EDRF effects. Hemoglobin contracts pig coronary arteries in vitro. However, during this contraction, effects of substance P and bradykinin which act via the EDRF are not inhibited. This means that the hemoglobin contraction is not caused by inhibition of the EDRF. This contraction is caused by a substance released from the endothelium, and by eicosanoïds released from the smooth muscles.

[Family food basket. Definition and methodology]. / Canasta familiar de alimentos. Definición y metodología.

A simple and practical methodology is proposed to define the "Family Food Basket", that must be based on the prevalent food situation of a country. At present, the "Family Food Basket" is an expression frequently used by government agencies (Ministries of Economics, Agriculture and Statistical Offices), because the money value estimation of the "Basket" is used as the basis for the establishment of minimum wages for the different socioeconomic groups. It is necessary, therefore, to determine the quantities of different foods that should be included as part of the diets so as to cover the nutritional requirements of the population. An explanation is also given here to show the differences between the "Food Basket" and the "Minimum Cost Recommended Diets", prepared in 1970 for the Central American countries. In order to explain the methodology, an example is given trying to define the "Family Food Basket of El Salvador" on the basis of available information gathered from food consumption surveys carried out at national level. Since a standardized methodology to obtain the actual food prices does not exist, some alternatives are given to estimate the money value of the "Family Food Basket".

Population and nutrition; implications of sociodemographic trends and differentials for food and nutrition policy in Central America and Panama.

PIP: This paper looks into some of the sociodemographic trends and differentials that may be influencing the lack of improvement in the food and nutrition situation in rural Central America. Evidence is presented that indicates that it is more difficult to reduce malnutrition and fertility than it was to reduce infant and child mortality initially. When sociostructural changes are not forthcoming after the initiation of the mortality decline, then resultant population growth, distribution and composition dynamics can hinder improvement in nutrition. In particular, changes in the social composition differentials as a result of selectivity in mortality, fertility and migration have apparently contributed to the increasing nutrition gap between the well-fed and the poorly-fed classes.^ieng