Systemic and centrally mediated angiotensin II effects in the horse

Abstract

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.

Hyperthermia Alters Kidney Function and Renal Scintigraphy

“…It was established that the output of ADH, aldosterone and renal function are affected by raising body temperature in experimental animals [3,8,9,10, 14]. There is a transient increase in the output of ADH and aldosterone, and decreased in kidney function during hyperthermia.…”

“…It is known that during hyperthermia the antidiuretic hormone (ADH) and aldosterone increased in plasma and this increase is proportional to the body temperature. These two hormones are essential to determine the amount of urine formation [8,9,10]. …”

Water Homeostasis and Diabetes Insipidus in Horses

“…Both osmotic and hemodynamic stimuli can produce their dipsogenic effect, in part, by activating a local reninangiotensin-aldosterone system in the central nervous system. 4,14,15 Studies in horses, ponies, and donkeys have shown that both increased P osm (induced by water deprivation or infusion of hypertonic saline) and hypovolemia (induced by furosemide administration) are stimuli for thirst. [16][17][18][19][20] As mentioned earlier, after a period of water deprivation, dehydrated equids seem to be able to replace water deficits within 15 to 30 minutes of gaining access to water.…”

Effect of oral administration of electrolyte pastes on rehydration of horses

“…Intravenous infusion of angiotensin II can induce drinking in horses, but supraphysiologic plasma concentrations of angiotensin II must be produced before thirst is stimulated. 28 To examine factors that may have stimulated thirst during dehydration and rehydration in the horses reported here, changes in body weight (reflecting the magnitude of water loss) and plasma tonicity (plasma sodium concentration) were compared with WI after dehydration and after oral administration of electrolyte pastes. Because furosemide administration and withholding of water overnight caused loss of water and electrolytes, only a modest increase in plasma sodium concentration was produced (approx 2 mmol/L [1.5%]).…”