The selective response to adenosine of renal microvessels from hamster explants.

The present study was undertaken to investigate the effect of adenosine on the microvasculature of the hamster kidney and the possibility of angiotensin II mediation. Renal tissue from neonatal hamsters was grafted into the cheek pouch of 33 adult hamsters. Seven to twelve days later the renal microcirculation was studied. Adenosine was tested on the pre- and postglomerular arterioles as well as on cheek pouch arterioles before and after applying an AII antagonist, saralasin. Adenosine dilated the cheek pouch arterioles and constricted the preglomerular arterioles in a dose-dependent manner. Adenosine had no effect on postglomerular arterioles. The renal vasoconstriction persisted as long as adenosine was present. Theophylline reduced the adenosine-mediated vasoconstriction of the afferent arteriole in a dose-dependent manner. These changes were not altered in the presence of saralasin at various doses, one of which was 20-fold greater than that required to abolish the vasoconstrictor response of a test dose of angiotensin II. This study indicates that the adenosine-mediated vasoconstriction of the preglomerular microvessels is not mediated via the renin-angiotensin system but may be a direct effect of adenosine.

Specificity of arginine vasopressin and angiotensin II for microvessels in the hamster cheek pouch after the induction of renovascular hypertension.

The present study was undertaken to determine the specificity of the vasoconstrictor activity to angiotensin II (AII) and arginine vasopressin (AVP) on the microcirculation in normal and renovascular hypertensive states. Ten to fourteen days after the induction of hypertension, Syrian hamsters were anesthetized with pentobarbital sodium, the cheek pouch was exposed, and a plastic chamber was placed in situ so the membrane could be suffused with bicarbonate-buffered Ringer's solution (5% CO2, 95% N2, pH 7.4). Third order arterioles (30-45 micron) were identified for study and vessel diameter was measured using a shearing device. In one group of normotensive and hypertensive hamsters, AII was microapplied to the arteriole before and after adding an AVP antagonist to the suffusate. In a second group of similar hamsters, AVP was microapplied to the arteriole before and after adding an angiotensin II blocker, saralasin acetate, to the suffusate. AVP and AII receptor blockade was documented by observing whether the vasoconstrictor effect of either AVP or AII was abolished. Dose-response curves for either peptide were not altered in the presence of the antagonist to the other peptide; however, they were shifted to the left in the RHT hamsters. Neither AVP nor AII receptor blockade altered control resting arteriolar diameters. Thus, it can be concluded that the microvascular response to both AII and AVP are potentiated in RHT and there are no interactions between either AII or AVP with the receptors of the other peptide in these microvessels in normal or RHT hamsters, indicating a high specificity for each peptide to its vascular receptor.

Comparative reactivity of hamster cheek pouch microvessels to arginine vasopressin and angiotensin II.

Experiments were carried out to determine the relative sensitivity of hamster cheek pouch vessels to arginine vasopressin (AVP) and angiotensin II (AII). Hamsters were anesthetized with pentobarbital sodium (6 mg/100 g, ip), a plastic chamber inserted into the cheek pouch and the membrane exposed. The membrane was suffused continuously with bicarbonate-buffered Ringer's solution at 36 degrees C while constantly monitoring blood pressure. After stabilization (30 min) of the membrane, arterioles (30-80 microM diam) were selected for application of AVP or AII in a random fashion. The peptides were applied to the vessels through a micropipette (10-15 mM tip diam) over two minutes using a pump. Total volume delivered was always 20 microliters irrespective of the total amount of peptide (10(0)-10(-4) ng) applied. Vessel diameter was monitored continuously with a shearing device before, during and after the administration of the peptide. The following results were obtained tachyphylaxis was noted to AII but to AVP; the dose response curve for AVP was shifted to the left of that for AII with the threshold dose for AII one hundred times more than that of AVP and AVP had little effect on venules whereas AII produced venoconstriction. These results indicate that AVP is a more potent vasoconstrictor than AII, whereas AII is a more potent venoconstrictor.