Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats

Abstract

. Regulation of plasma vasopressin and renin activity in conscious hindlimb-unloaded rats. Am J Physiol Regul Integr Comp Physiol 291: R46 -R52, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00622.2005.-Cardiovascular deconditioning occurs in astronauts after spaceflight or in individuals subjected to bed rest. It is characterized by an increased incidence of orthostatic intolerance. The mechanisms responsible for orthostatic intolerance are likely multifactorial and may include hypovolemia, autonomic dysfunction, and vascular and cardiac alterations. The arterial baroreflex is an important compensatory mechanism in the response to an orthostatic stress. In a previous study, we demonstrated that arterial baroreflex mediated sympathoexcitation was blunted in hindlimb-unloaded (HU) rats, a model of cardiovascular deconditioning. The arterial baroreflex also contributes to the regulation of vasoactive hormones including vasopressin and angiotensin II. In the present study, we tested the hypothesis that the neurohumoral response to hypotension is also attenuated in rats after 14 days of hindlimb unloading. To test this hypothesis, the vasodilator diazoxide (15 or 25 mg/kg) or saline (0.9%) was administered to produce hypotension or control conditions, respectively, in conscious HU and control rats. Plasma samples were collected and assayed for vasopressin and plasma renin activity (PRA). Diazoxide (25 mg/kg) produced significant increases in vasopressin and PRA compared with saline controls. HU rats exhibited significantly higher levels of vasopressin at rest and the increase in vasopressin levels during hypotension was enhanced by hindlimb unloading. Neither resting nor hypotension-induced PRA was altered by hindlimb unloading. These data suggest that although baroreflex-mediated sympathoexcitation is blunted by hindlimb unloading, hypotension-induced vasopressin release is enhanced and hypotension-induced PRA is unaffected. Increased circulating vasopressin may serve to compensate for blunted baroreflex regulation of sympathetic nervous activity produced by hindlimb unloading or may actually contribute to it. neurohumoral control; antidiuretic hormone; renin-angiotensin system ASTRONAUTS RETURNING FROM space, or individuals recovering from prolonged bed rest often experience symptoms of orthostatic intolerance (5,8,16,31,54,65). To delineate the possible mechanisms mediating orthostatic intolerance, individuals have been categorized as presyncopal or nonpresyncopal (17, 31, 66), finishers and nonfinishers (5), or simply, orthostatic tolerant and intolerant (54). No matter what nomenclature is used, the common characteristic among these individuals is an inability to maintain arterial pressure during an orthostatic challenge.Compensations for orthostatic stress include baroreflexmediated increases in heart rate in an attempt to maintain cardiac output, as well as increases in total peripheral resistance to maintain adequate arterial pressure (47). Initially, vasoconstriction is accomplished through a...

Influence of sedentary versus physically active conditions on regulation of plasma renin activity and vasopressin

“…For example, regulation of AVP has been reported to be altered in sedentary compared with endurance-trained subjects (8,17). In addition, we previously reported differential effects of hindlimb unloading on baroreflex-mediated sympathoexcitation, activation of the renin-angiotensin system, and vasopressin secretion (29,35). Therefore, on the basis of the previous observations that sedentary vs. physically active conditions enhance baroreflex-mediated sympathoexcitation (6,13,36), we hypothesized that regulation of the renin-angiotensin system and AVP secretion would be enhanced in sedentary vs. physically active rats.…”

“…In addition to sympathoexcitation, the response to baroreceptor unloading is also associated with activation of the renin-angiotensin system and increased plasma concentrations of vasoactive hormones such as angiotensin and AVP (35,42,47,48). It is possible that regulation of the renin-angiotensin system or vasopressin secretion is altered by physical activity or inactivity.…”

Neural and humoral control of regional vascular beds via A1 adenosine receptors located in the nucleus tractus solitarii

“…This could attenuate further increases of these vasoactive factors due to stimulation of NTS A 1 adenosine receptors. In fact, in our previous study, which was performed under similar experimental conditions, the resting vasopressin levels were moderately elevated compared with the levels measured in conscious animals (5,15,18,(25)(26)(27). Nevertheless, the activation of NTS A 1 adenosine receptors evoked a large (Ͼ4-fold) increase of circulating vasopressin compared with the elevated baseline (25).…”

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

“…Such potentiation of the increases in ADH and NE might be due to the cardiovascular-regulating system showing compensatory or hypersensitive responses as a result of a lack of afferent inflow from the kidneys. Such enhancements in ADH and plasma NE responses have been seen in spaceflight (45) and in hindlimbunloaded animals (49,64). Indeed, mechano-and chemosensitive information transmitted from the kidneys to the paraventricular nucleus (PVN) of the hypothalamus via the renal afferent nerves has been shown to contribute to the modulation of ADH release (14,58,60).…”