The primary aim of the study was to evaluate the potential value of intravenous (i.v.) infusion of angiotensin II (AII) for phonocardiographic differential diagnosis of equine valvular insufficiency. Ten-minute AII infusions at 4.5-33 pmol kg-1 min-1 induced clear-cut dose-dependent rises in systemic arterial blood pressure (aBP), whereas the pulmonary aBP remained largely unaffected. It implies that i.v. infusion of AII at about 10 pmol kg-1 min-1 could be a valuable tool for the acoustic differentiation between mitral and tricuspid valvular dysfunction in the horse. The infusion at, and above 9 pmol kg-1 min-1 caused increased heart rate. This chronotrophic effect was not strictly dose-dependent and exhibited significant tachyphylaxis. Angiotensin II administration at, or above 9 pmol kg-1 min-1 was needed to induce an urge to drink, suggesting that angiotensin-induced thirst does not appear in the euhydrated horse until the octapeptide reaches supraphysiological blood concentration. Determinations of plasma aldosterone concentration (PA) revealed comparatively high morning control values (269 +/- 46 pmol-1). Three consecutive AII infusions with 10-min intervals and at increasing dosages caused a cumulative, almost fourfold elevation of PA. The PA pattern indicated that AII-induced hypersecretion of aldosterone continued for several minutes after the end of the infusions, but also showed that the metabolic clearance of the hormone took precedency of the secretion within 20 min post-infusion. In two of the horses a fall in PA occurred during a fourth, final infusion, indicating that in these instances the previous AII administration had impoverished the store of aldosterone available for release from the adrenal cortex.

Metabolic and respiratory alkalosis were produced in goats with the primary aim of studying possible influence of a reduced blood hydrogen ion concentration on aldosterone secretion. Metabolic alkalosis was induced by 1 h i.v. infusion of hypertonic tris(hydroxy-methyl)aminomethane (THAM) solution. The infusion was associated with a significant reduction in plasma aldosterone concentration (PA). It occurred in the absence of a detectable fall in plasma K or obvious change in plasma renin activity, but simultaneously with a moderate increase in plasma cortisol concentration and a significant reduction of plasma Na concentration. It suggests that changes of the primary aldosterone regulators were not the cause of the fall in PA, but leaves open the possibility that either the decreased blood hydrogen ion concentration as such or THAM-induced blood hypertonicity reduced the aldosterone secretion. The respiratory alkalosis was due to heat polypnoea elicited by 2 h exposure of the goats to 45 degrees C. Here, no obvious change in PA was observed during the alkalotic period, which, however, was associated with a rise in plasma K. Increased K stimulation may therefore have masked a possible inhibitory influence of the alkalosis upon the aldosterone secretion.

The influence of bilaterally narrow, medial forebrain lesions on the increase in plasma cortisol concentration normally seen in response to intravenous angiotensin II was studied in five goats. For comparison, the pre- and post-lesion cortisol responses to intravenous endotoxin were also evaluated. The cortisol response to angiotensin was extinguished in two goats, whereas a slightly attenuated response to endotoxin was still obtained post-lesioning. In these animals the lesions embraced the subfornical organ (SFO), the organum vasculosum of the lamina terminals (OVLT) and the interjacent anterior wall of the third ventricle. In two other goats, in which the SFO was completely destroyed but the OVLT remained largely intact, the lesions caused about 50% reduction of the cortisol response to angiotensin without any concomitant reduction of the response to endotoxin. It is concluded that ACTH-cortisol release in response to systemic angiotensin II is not mediated exclusively by receptors for the octapeptide confined to the SFO. Angiotensin receptors in the OVLT seem to be equally important in this respect.

Intracerebroventricular (ICV) infusion of the competitive inhibitor for angiotensin II (AII), saralasin, (13 pmol kg-1 min-1), preceding and outlasting the intravenous (i.v.) infusion of AII (40 pmol kg-1 min-1) extinguished the elevation in plasma cortisol (PC) obtained in response to just the i.v. AII infusion. The corresponding i.v. infusion of saralasin did not visibly influence the AII-induced elevation of PC, whereas bilateral intracarotid infusions of the inhibitor tended to reduce the response. The ICV administration of the inhibitor also significantly reduced the rise in plasma aldosterone (PA) seen as an effect of the i.v. AII. Paradoxically, however, the intravascular infusions of saralasin conspicuously augmented the rise in PA obtained after the simultaneous i.v. infusion of AII. It is concluded that cerebral mediation of the ACTH-cortisol response to systemic AII occurs at sites accessible to inhibition from both sides of the blood-brain barrier, and that also the PA response to blood-borne AII may be to some extent cerebrally mediated.

The influence of cerebrospinal fluid (CSF) NaCl concentration upon the cortisol release induced by intracerebroventricular (i.c.v.) and intravenous (i.v.) infusions of angiotensin II (AII) was studied in conscious goats. A first series of experiments involved i.c.v. infusion (20 min; 20 microliters min-1) of simply hypertonic (0.5 M) NaCl, or of AII (2 pmol kg-1 min-1) dissolved in 0.5 M or isotonic (0.15 M) NaCl or in isotonic glucose. The most pronounced rise in plasma cortisol concentration (PC) was elicited by AII in 0.5 M NaCl, but responses of nearly the same size were obtained by merely 0.5 M NaCl and by AII in isotonic NaCl, whereas AII in glucose induced a smaller PC rise. An urge to drink developed during all infusions, except during the AII/glucose infusion. Here, however, thirst became apparent 2-6 min post-infusion. When, in a second series, the hypertonicity of the NaCl was reduced to 0.3 M, and the dose of AII to 0.5 pmol kg-1 min-1, only the infusion of AII in 0.3 M NaCl elicited any appreciable rise in PC. The response was approximately the same size as that earlier obtained as the effect of the larger dose of AII dissolved in isotonic saline. In a third series of experiments, a 30-min i.c.v. infusion of isotonic glucose, preceding and out-lasting a 10-min i.v. infusion of AII (40 pmol kg-1 min-1), was found to extinguish the rise in PC obtained as the effect of a separate i.v. infusion of AII.(ABSTRACT TRUNCATED AT 250 WORDS)