Pressor action of intravenous angiotensin II reduces drinking response in rats

Robinson, Marilyn M.; Evered, Mark

doi:10.1152/ajpregu.1987.252.4.r754

Cited by 50 publications

(37 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, several investigators have postulated that the pressor action of exogenously administered ANG II masks the ability of ANG II to stimulate thirst, vasopressin secretion, and sympathetic outflow. In this regard, barodenervation or prevention of the ANG II-evoked increase in ABP does enhance thirst and acutely increases sympathetic outflow (Robinson and Evered, 1987;Schreihofer et al, 2000;Stocker et al, 2001Stocker et al, , 2002Xu and Sved, 2002;Stocker et al, 2004). To the extent it has been examined, similar observations have been reported during increases in plasma osmolality (Weiss et al, 1996;Chen and Toney, 2001;Stocker et al, 2001Stocker et al, , 2002.…”

Section: Discussionmentioning

confidence: 75%

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Stocker

Toney

2007

Brain Research

View full text Add to dashboard Cite

The goal of the present study was to determine the effect of activating vagal afferent fibers on the discharge of median preoptic (MnPO) neurons responsive to peripheral angiotensin II (ANG II) and osmotic inputs. Vagal afferents were activated by electrical stimulation of the proximal end of the transected cervical vagus nerve (3 pulses, 100 Hz, 1 ms, 100-500 μA). Of 21 MnPO neurons, 19 were antidromically activated from the hypothalamic paraventricular nucleus (PVH) (latency: 10.3 ±1.3 ms, threshold: 278±25 μA). MnPO-PVH cells had an average spontaneous discharge of 2.1±0.4 Hz. Injection of ANG II (150 ng) and/or hypertonic NaCl (1.5 Osm/L, 100 μl) through the internal carotid artery significantly (P<0.01) increased the firing rate of most 84%). Vagus nerve stimulation significantly (P<0.01) decreased discharge (−73±9%) in 10 of 16 (63%) neurons with an average onset latency of 108±19 ms. Among the remaining 6 MnPO-PVH neurons vagal activation either increased discharge (177±100%) with a latency of 115±15 ms (n=2) or had no effect (n=4). Pharmacological activation of chemosensitive vagal afferents with phenyl biguanide produced an increase (n=3), decrease (n=2), or no change (n=6) in discharge. These observations indicate that a significant proportion of ANG II-and/or osmo-sensitive MnPO neurons receive convergent vagal input. Although the sensory modalities transmitted by the vagal afferents to MnPO-PVH neurons are not presently known, the presence of inhibitory and excitatory vagalevoked responses indicates that synaptic processing by these cells integrates humoral and visceral information to subserve potentially important cardiovascular and body fluid homeostatic functions.

show abstract

Section: Discussionmentioning

confidence: 75%

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

Stocker

Toney

2007

Brain Research

View full text Add to dashboard Cite

show abstract

“…Drinking caused by minoxidil is largely renin dependent. As with drinking in response to diazoxide (10,31), drinking after minoxidil is blocked by treatment with an angiotensin-converting enzyme inhibitor (e.g., captopril; 31, 39). Minoxidil stimulates renin secretion by baroreflex activation of renal sympathetic (␤-adrenergic receptor-mediated) nerves (27).…”

Section: Discussionmentioning

confidence: 99%

Hypotension- and osmotically induced thirst in old Brown Norway rats

Thunhorst¹,

Beltz²,

Johnson³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Thunhorst RL, Beltz TG, Johnson AK. Hypotension-and osmotically induced thirst in old Brown Norway rats. Am J Physiol Regul Integr Comp Physiol 297: R149 -R157, 2009. First published May 6, 2009 doi:10.1152/ajpregu.00118.2009.-Compared to young cohorts, old rats drink less water in response to several thirst-inducing stimuli. In these experiments, we characterized water drinking in response to hypotension and cellular dehydration in young (4 mo), middle-aged adult (12 mo) and old (29 -30 mo) male Brown Norway rats. We injected the vasodilator, minoxidil as an intravenous bolus in a range of doses (0 -20 mg/kg), so that drinking responses could be compared at equivalent reductions of arterial pressure. Old rats had greatly diminished reflex tachycardia and became significantly more hypotensive after minoxidil compared with young and middle-aged rats. When compared at equivalent reductions of arterial pressure, old rats drank one-third as much as middle-aged rats, and one-fifth as much as young rats. In addition, there were age-related deficits in drinking in response to a range of administered loads of sodium (0.15-2 M NaCl, 2 ml/100 g body wt). Urinary excretion of water and sodium in response to the loads was equivalent across ages. Both middle-aged and old rats were less able than young rats to repair their water deficits after sodium loading, attributable almost entirely to their reduced drinking responses compared with young rats. Lastly, agerelated declines in drinking appeared to be more severe in response to hypotension than in response to cellular dehydration. aging; drinking; diuresis; natriuresis; dehydration; blood pressure; heart rate ELDERLY PEOPLE AND OLD ANIMALS have impaired drinking responses to many thirst-inducing challenges (21, 23, 25, 28, 29, 33-35, 40, 41). However, the nature of the underlying causes of reduced drinking that accompanies old age, such as impaired neural or humoral signaling mechanisms, remain largely undetermined. Knowledge of the causes of age-related declines in drinking will increase our understanding of the ways to help the elderly maintain better fluid homeostasis. This is an important consideration for an increasingly aging population and for the relationship between hydrational status and disorders, such as heat-related injury.Hypotension is a potent stimulus of thirst in rats (e.g., 10,17,18,26,30,38). Thirst following hypotension is due mainly to release of renin and formation of ANG II in the circulation (26, 38; for a review, see Ref. 20) and is blocked by interfering with the actions of, or formation of, ANG II (10,26,33,38). There are conflicting reports about whether old rats drink less in response to hypotension. For example, old rats have been found to drink less after subcutaneous injections of isoproterenol compared with young rats (24, 34, 37), although not always (25,34). These previous studies did not record arterial pressure or control for differences in arterial pressure that may occur with aging (24,25,34,37). This information is important becau...

show abstract

“…Such an inhibitory effect has been demonstrated in rats, 63 but would not be expected to result from increased endogenously-generated Ang II which occurs under physiological conditions of hypovolaemia or sodium depletion, where BP does not rise. Evidence that is suggestive of a central dipsogenic effect of circulating Ang II in humans is the intense thirst observed in patients with chronic renal failure undergoing intermittent renal haemodialysis.…”

Section: Thirstmentioning

confidence: 90%