scholarly journals Drinking and arterial blood pressure responses to ANG II in young and old rats

2010 ◽  
Vol 299 (5) ◽  
pp. R1135-R1141 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Ang Ii ◽  
Middle Aged ◽  
Reduced Pressure ◽  
Water Drinking ◽  
Young Rats ◽  
Arterial Blood ◽  
Old Rats ◽  
Blood Pressure Responses

We investigated water drinking and arterial blood pressure responses to intravenous infusions of ANG II in young (4 mo), middle-aged adult (12 mo), and old (29 mo) male Brown Norway rats. Infusions of ANG II began with arterial blood pressure either at control levels or at reduced levels following injection of the vasodilator minoxidil. Under control conditions, mean arterial pressure (MAP) in response to ANG II rose to the same level for all groups, and middle-aged and old rats drank as much or more water in response to ANG II compared with young rats, depending on whether intakes were analyzed using absolute or body weight-adjusted values. When arterial blood pressure first was reduced with minoxidil, MAP in response to ANG II stabilized at significantly lower levels compared with control conditions for all groups. Young rats drank significantly more water under reduced pressure conditions compared with control conditions, while middle-aged and old rats did not. Urine volume in response to ANG II was lower, while water balance was higher, under conditions of reduced pressure compared with control conditions. Baroreflex control of heart rate was substantially reduced in old rats compared with young and middle-aged animals. In summary, young rats appear to be more sensitive to the inhibitory effects of increased arterial blood pressure on water drinking than are older animals.

scholarly journals Effects of β-adrenergic receptor agonists on drinking and arterial blood pressure in young and old rats

2011 ◽  
Vol 300 (4) ◽  
pp. R1001-R1008 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Connie L. Grobe ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Aged Rats ◽  
Middle Aged ◽  
Young Rats ◽  
Arterial Blood ◽  
Age Related ◽  
Old Rats

These experiments examined water-drinking and arterial blood pressure responses to β-adrenergic receptor activation in young (4 mo), “middle-aged” adult (12 mo), and old (29 mo) male rats of the Brown-Norway strain. We used isoproterenol to simultaneously activate β1- and β2-adrenergic receptors, salbutamol to selectively activate β2-adrenergic receptors, and the combination of isoproterenol and the β2-adrenergic receptor antagonist ICI 118,551 to stimulate only β1-adrenergic receptors. Animals received one of the drug treatments, and water drinking was measured for 90 min. About 1 wk later, animals received the same drug treatment for measurement of arterial blood pressure responses for 90 min. In some rats, levels of renin and aldosterone secretion in response to isoproterenol or salbutamol were measured in additional tests. Old and middle-aged rats drank significantly less after isoproterenol than did young rats and also had greater reductions in arterial blood pressure. Old and middle-aged rats drank significantly less after salbutamol than did young rats, although reductions in arterial blood pressure were equivalent across the ages. The β2-adrenergic antagonist ICI 118,551 abolished drinking after isoproterenol and prevented most of the observed hypotension. Renin secretion after isoproterenol and salbutamol was greater in young rats than in middle-aged rats, and wholly absent in old rats. Aldosterone secretion was reduced in old rats compared with young and middle-aged rats after treatment with isoproterenol, but not after treatment with salbutamol. In conclusion, there are age-related differences in β-adrenergic receptor-mediated drinking that can be explained only in part by age-related differences in renin secretion after β-adrenergic receptor stimulation.

Tempol improves vascular function in the mesenteric vascular bed of senescent rats

2004 ◽  
Vol 82 (3) ◽  
pp. 200-207 ◽  
Author(s):  
R Tatchum-Talom ◽  
D S Martin
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Function ◽  
Chronic Treatment ◽  
Young Rats ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Old Rats ◽  
Mesenteric Vascular Bed

Ageing is associated with structural and functional alterations of the vasculature. The nature of age-related vascular disorders is not completely understood. Oxidative stress is hypothesized to play a crucial role in the pathophysiology of vascular complications. We investigated the effects of chronic treatment with the superoxide dismutase mimetic tempol (4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl) on vascular function in the mesenteric vasculature of aged rats. Young (3 weeks) and old (40 weeks) Sprague–Dawley rats were treated with tempol (1 mM in drinking water) or vehicle for 3 weeks. Arterial blood pressure was slightly, but significantly, higher in old than in young rats. Tempol had no effect on arterial blood pressure. The vasoconstrictor responses to norepinephrine (NE) and serotonin (5-HT) were exaggerated in the mesenteric vascular bed (MVB) removed from old rats. Vasodilator responses to acetylcholine (ACh), papaverine (PPV), and isoprenaline (ISO) were reduced in the MVB of old rats in comparison with young rats. Chronic treatment of old rats with tempol normalized their responses to NE and 5-HT. The dilator responses to ACh, PPV, and ISO were similar between old rats receiving tempol and young rats. The present findings suggest that oxidative stress contributes to vascular dysfunction in the mesentery of old rats. The vasculoprotective effects of tempol remain to be elucidated.Key words: ageing, oxidative stress, vascular reactivity.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Functional Interaction between Angiotensin and Sympathetic Reflexes in Cats

1982 ◽  
Vol 62 (1) ◽  
pp. 51-56 ◽  
Author(s):  
R. Hatton ◽  
D. P. Clough ◽  
S. A. Adigun ◽  
J. Conway
Keyword(s):  
Blood Pressure ◽  
Central Venous Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Partial Recovery ◽  
Ang Ii ◽  
Central Venous ◽  
Efferent Nerve ◽  
Arterial Blood ◽  
Sympathetic Reflexes

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At −50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9–3.2 ng h−1 ml−1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8]ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.

Arterial baroreceptors mediate the inhibitory effect of acute increases in arterial blood pressure on thirst

2002 ◽  
Vol 282 (6) ◽  
pp. R1718-R1729 ◽  
Author(s):  
Sean D. Stocker ◽  
Edward M. Stricker ◽  
Alan F. Sved
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Drinking Behavior ◽  
Plasma Osmolality ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Arterial Blood ◽  
Acute Increase ◽  
Behavior Of Rats ◽  
Arterial Baroreceptor

The present study sought to determine whether arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in arterial blood pressure (AP) on thirst stimulated by systemically administered ANG II or by hyperosmolality. Approximately 2 wk after sinoaortic denervation, one of four doses of ANG II (10, 40, 100, or 250 ng · kg−1 · min−1) was infused intravenously in control and complete sinoaortic-denervated (SAD) rats. Complete SAD rats ingested more water than control rats when infused with 40, 100, or 250 ng · kg−1 · min−1 ANG II. Furthermore, complete SAD rats displayed significantly shorter latencies to drink compared with control rats. In a separate group of rats, drinking behavior was stimulated by increases in plasma osmolality, and mean AP was raised by an infusion of phenylephrine (PE). The infusion of PE significantly reduced water intake and lengthened the latencies to drink in control rats but not in complete SAD rats. In all experiments, drinking behavior of rats that were subjected to sinoaortic denervation surgery but had residual baroreceptor reflex function (partial SAD rats) was similar to that of control rats. Thus it appears that arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in AP on thirst stimulated by ANG II or hyperosmolality.

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