Hemodynamics of central infusion of angiotensin II in normal and sodium-depleted dogs

Abstract

The intraventricular (IVT) administration of angiotensin II (AII) (100 ng.kg-1.min-1) produced significant elevations of arterial blood pressure in pentobarbital-anesthetized dogs on either normal or sodium-deficient diets. In both groups of dogs the intraventricular administration of AII caused comparable and significant elevations in blood pressure averaging 15 +/- 2 and 17 +/- 4 mmHg, respectively, within 10 min after onset of the infusion. The rises in blood pressure were due to increased peripheral resistance (2.87 +/- 1.20 vs. 1.67 +/- 0.43 units). At the peak of the pressor response bradycardia was a constant feature in sodium-depleted animals, but was not present in the normal ones. In both groups of dogs regional cerebral blood flow (rCBF), determined by the xenon-133 washout method, remained unchanged during the development of the pressor response, and peripheral plasma renin activity failed to increase in response to the central infusion of AII. In conclusion, sodium deprivation appears not to influence the sensitivity of the central AII receptor because comparable pressor responses and hemodynamic changes were obtained following the intraventricular administration of AII in both normal and sodium-depleted dogs.

The effect of analogues of angiotensin II on drinking and cardiovascular responses to central angiotensin II in the rat.

“…These results agree with those obtained by Hoffman & Phillips (1976) and Colombari, Saad, Camargo, Renzi, De Luca & Menani (1990). A series of observations have indicated that the action of this peptide in inducing a pressor response is due to the activation of the receptors at many sites in the brain (Zimmerman, 1973(Zimmerman, , 1978Anderson, 1977;Simpson, Epstein & Camargo, 1978;Brosnihan, Berti & Ferrario, 1979). Another possible action of Isoleu5-AngII is the activation of the release of a cerebral hormone with a prolonged vasopressor effect.…”

Central angiotensin II-induced pressor responses and neural activity in utero and hypothalamic angiotensin receptors in preterm ovine fetus

“…Fetal heart rate was decreased during the same period and was further decreased to significantly slower levels until 60 min after the intracerebroventricular injections. Whereas the pressor effect of intracerebroventricular ANG II has been well established, the response of heart rate to central ANG depends on species, action sites, injection routes, and other conditions (3,4,13,20,25). For example, an intracerebroventricular injection of ANG II agonist induced a dose-dependent increase in heart rate and arterial BP in conscious trout (20).…”

“…Our recent studies have demonstrated an increase of fetal mean arterial pressure (MAP) immediately after an injection of ANG II into the lateral ventricle of the near-term (90% gestational age) ovine fetal brain in utero (36). This observation prompted initial experiments investigating the cardiovascular action of fetal intracerebroventricular injection of octapeptide ANG II.In the adult, administration of either ANG II or its precursors into the brain induces pressor responses, drinking, and release of hormones (3,11,29). A number of studies have confirmed that almost all biological effects of ANG II are expressed via angiotensin subtype 1 (AT 1 ) receptors, not AT 2 receptors (21, 31, 32).…”

“…In the adult, administration of either ANG II or its precursors into the brain induces pressor responses, drinking, and release of hormones (3,11,29). A number of studies have confirmed that almost all biological effects of ANG II are expressed via angiotensin subtype 1 (AT 1 ) receptors, not AT 2 receptors (21, 31, 32).…”

Role of Intracerebral Angiotensin Receptors in the Regulation of Vasopressin Release and the Cardiovascular System

“…Brosnihan et al [2] and Gildenberg et al [3] found that intracerebroventricular administration of a relatively large dose of Ang II (100 ng/kg/min or 100 ng in one bolus) was required to elevate arterial blood pressure in anesthetized dogs. Furthermore, Monianiet al (10] reported that a mod erate rise in plasma ADH level decreased cardiac output and heart rate via an enhancement of baroreceptor reflex in dogs and counteracted a rise in blood pressure.…”