The contribution of vasopressin and angiotensin to the maintenance of blood pressure after autonomic blockade.

Hiwatari, Masao; Nolan, Peter L.; Johnston, Colin I.

doi:10.1161/01.hyp.7.4.547

Cited by 27 publications

(13 citation statements)

References 29 publications

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“…It is known that the activity of the renin-angiotensin system is enhanced in DI rats, possibly as a means of compensating for the absence of AVP. 24 However, under the same experimental conditions as applied in the present study, Hiwatari et al 23 demonstrated that, after total autonomic blockade, blood pressure in DI rats was lower than that in LE rats, and the reninangiotensin system was activated more by autonomic blockade in the former. Therefore, higher blood pressure in DI rats may not be attributable to enhanced activity of the renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 43%

“…21 When one system is removed, its influence can be partially and sometimes completely compensated by increased activity in the remaining systems. 22 ' 23 Thus, the deficiency of circulating AVP in DI rats may not necessarily result in hypotension, but the relatively higher blood pressure levels observed in DI rats are not easily explained. Several possible mechanisms may be postulated.…”

Section: Discussionmentioning

confidence: 99%

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Cardiovascular depression and stabilization by central vasopressin in rats.

et al. 1990

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The role of endogenous vasopressin in cardiovascular homeostasis was examined using vasopressin-deftcient rats (Brattleboro) (n=194) and their parent strain, Long-Evans rats (n=181). Mean arterial pressure (blood pressure) and heart rate were measured every 4 seconds with or without infusion of drug solution for 21 hours, and mean values and their standard deviations (lability) were calculated. Blood pressure in Brattleboro rats (116±1.1 mm Hg, mean±SEM) was significantly higher than that in Long-Evans rats (96±0.7 mm Hg, /><0.001), whereas heart rates (381±33 and 375±2.9 beats/min, respectively) were similar. The lability of blood pressure and heart rate in Brattleboro rats (9.2±0.1 mm Hg and 42 J±0.7 beats/min) was also greater than that in Long-Evans rats (6.7 ±0.1 mm Hg, p< 0.001 and 38.4±0.8 beats/min, p<0.0l, respectively). In Brattleboro rats, intravenous vasopressin (0.1 ng/kg/min or 0.6 ng/kg/min) did not affect blood pressure, although it did reduce heart rate and decreased lability of blood pressure and heart rate. Intracerebroventricular (central) infusion of vasopressin (2 pg/kg/min) in Brattleboro rats induced initial hypertension and tachycardia followed by long-lasting hypotension and bradycardia, whereas in Long-Evans rats it induced only hypertension and tachycardia. In both strains, central vasopressin dramatically decreased the lability of blood pressure and heart rate. A rginine vasopressin (AVP) has long been known to possess potent vasoconstrictor properties. 1 However, when AVP is infused intravenously into conscious animals or humans, there is no increase in blood pressure until extremely high plasma AVP levels are achieved. 2 Evidence has accumulated indicating that the absence of increases in blood pressure in response to AVP infusion in normotensive animals may be due to the presence of an effective and specific buffering system. 3 -5 On the basis of available evidence, it has been proposed that the locus of this buffering system is in the central nervous system. 6 -12 Recently, it has been reported that Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI rats) have suppressed baroreceptor reflex sensitivity. 9 Exogenous AVP and the V 2 renal receptor agonist desmopressin (DDAVP) administered systemically is able to restore this suppressed sensitivity to within the range that is normal for Long-Evans (LE) rats. 9 It is believed that the inhibition of baroreceptor reflex pathway raises blood pressure. 13 Therefore, it may be postulated that rats with suppressed baroreceptor reflex mechanisms will have higher blood pressure and heart rate and a greater lability of blood pressure and heart rate than normal rats. Furthermore, we previously reported that centrally administered AVP lowered blood pressure in DI rats as well as in stroke-prone by guest on May 11, 2018 http://hyper.ahajournals.org/ Downloaded from

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Section: Discussionmentioning

confidence: 43%

Section: Discussionmentioning

confidence: 99%

Cardiovascular depression and stabilization by central vasopressin in rats.

et al. 1990

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“…Hiwatari et al 23 recently showed that immediately after pentolinium-induced autonomic block there was transient release of angiotensin II and vasopressin, which helped to maintain blood pressure. However, we believe that circulating hormones played only a small role in accounting for the response differences between hypertensive and normal rabbits, since (1) the elevations of hormone concentrations demonstrated by Hiwatari et al 23 were only transient and would be small 20 minutes after giving blocking drugs when we obtained our first doseresponse curve; (2) the differences in dose-vascular response curves between hypertensive and normal rabbits were similar with all drugs, some of which would produce differential changes in hormone concentrations; (3) there was no time-dependence on resting blood pressure and vascular resistance over the entire time course of the experiment.…”

Section: Discussionmentioning

confidence: 99%

Vascular amplifier properties in renovascular hypertension in conscious rabbits. Hindquarter responses to constrictor and dilator stimuli.

Wright¹,

Angus²,

Korner³

1987

Hypertension

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SUMMARY The local responses of the resistance vessels of the hindquarters of conscious, renal hypertensive (cellophane wrap) and sham-operated normotensive rabbits were studied during infusions of constrictor (norepinephrine, methoxamine, angiotensin II) and dilator (acetylcholine, adenosine, serotonin) drugs. The rabbits had implanted Doppler ultrasonic flow probes on the lower aorta and an indwelling catheter for intra-arterial infusion of drugs. Autonomic blockade with mecamylamine and propranolol was used to determine local vascular effects of each drug uncomplicated by reflex changes. Logistic dose-vascular response curves were characterized by (1) their range from resting to maximum response, (2) their 50% effective dose (i.e., sensitivity or dose at middle of the response range), and (3) the average slope about the 50% effective dose. At maximum dilatation the vascular resistance was about 70% greater in hypertensive rabbits than in normotensive rabbits. There were no significant differences in 50% effective dose values between curves for hypertensive and normotensive rabbits for constrictor or dilator drugs. However, with all drugs the hypertensive rabbits showed about twice the change in vascular resistance per unit dose compared with the normotensive rabbits. These results suggest that hypertrophy of the muscles of the precapillary vessels makes them a nonspecific amplifier of vascular resistance changes evoked by constrictor and dilator stimuli. They do not support previous claims of specific changes in "sensitivity" or claims that local amplifier action is unimportant in hypertension. (Hypertension 9: 122-131, 1987) KEY WORDS reactivity amplifier properties • constrictors • dilators * hypertension • vascular T HE amplifier properties of the hypertrophied vascular and cardiac musculature in primary and many types of secondary hypertension have been considered to play a role in the hemodynamic patterns of hypertension and most circulatory responses.1 ' 2 Folkow et al. 3 pointed out that the associated increase in the ratio of the wall thickness to lumen radius was important in making the small arteries and arterioles hemodynamic amplifiers of stimuli affecting vascular resistance. As a result, a given dose of constrictor agent or a given percentage shortening of the muscle would produce more pronounced vascular narrowing in hypertension than in normal vessels. This response has now been demonstrated in the isolated vessels of the limb and kidney in spontaneously hyper- Received October 1, 1985; accepted August 19, 1986. tensive rats (SHR), in rats with renal hypertension, and in the cutaneous circulation of patients with primary hypertension. 12 We have confirmed these amplifier properties in conscious rabbits with established renovascular (cellophane wrap) hypertension in which reflex influences on the circulation were abolished by autonomic blockade. 4 Moreover, we found similar enhancement of responsiveness to norepinephrine, angiotensin II, and vasopressin, which is in accord with nonspecific...

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“…Baroreceptors, present in the adventitia of conduit vessels such as the aorta and carotid arteries, may reset as a consequence of alterations in vessel distensibility (Koushanpour, 1991). GTN is known to increase arterial compliance (Sumimoto et al, 1993) (Hiwatari et al, 1985). Further studies are required to examine the involvement of these neurohumoral effectors in modulating the dose dependence of the depressor action of GTN.…”

Section: Rabbit Body Weightmentioning

confidence: 99%

Baroreflex resetting but no vascular tolerance in response to transdermal glyceryl trinitrate in conscious rabbits

Serone

Angus

Wright

1996

British J Pharmacology

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1 We investigated whether acute (5 h) and chronic (3 days) transdermal glyceryl trinitrate (GTN) patches could cause the development of tolerance in terms of haemodynamics and vascular reactivity in the conscious rabbit. The effects of haemodynamic tolerance were assessed on arterial pressure, heart rate and the baroreflex control of heart rate, while hindquarter vascular reactivity in response to dilator and constrictor drugs and reactive hyperaemia were used to assess vascular tolerance. 2 Seven days prior to experiments, an inflatable cuff, a pulsed Doppler flow probe and an indwelling intra-aortic catheter (for i.a. agonist infusions) were implanted around the lower abdominal aorta. 3 In acute experiments, the effects of 0-5 h treatment with transdermal GTN (0 Sham), 10 or 20 mg 24 h-') on MAP, HR and the baroreflex were examined. Chronic experiments were performed on three separate days (days 0 -before, 4 -with GTN patch and 8 -recovery). On each day, the baroreflex, reactive hyperaemic responses and hindquarter vascular dose-response curves to i.a. GTN, adenosine, acetylcholine, S-nitroso-N-acetylpenicillamine (SNAP) and methoxamine were assessed. On days 1-4, GTN was administered transdermally via a patch(es) (10 mg 24 h-' (low dose) or 20 mg 24 h-' (high dose); renewed every 24 h). 4 Acute treatment with 20 mg GTN 24 h', but not with 0 (n=4) or 10 mg GTN 24 h-' (n=4), caused a significant fall in MAP (-8+1 mmHg; n = 4) and resetting of the baroreflex by 5 h. Chronic GTN caused a significant fall in MAP of 8 + 2 and 8 + 2 mmHg on day 4 with low (n = 8) and high dose (n = 8), respectively, with no change in HR. There was no significant change to hindquarter vascular reactivity to i.a. infusion of GTN, nor were there any significant differences in the reactivity to i.a. adenosine, acetylcholine, SNAP or methoxamine with either low or high doses of GTN. 5 Chronic GTN treatment with low and high dose patches caused a parallel leftward shift ('resetting') of the baroreflex on day 4. By day 8, the baroreflex had still not recovered from this leftward shift. 6 In the rabbit, chronic exposure to clinical nitrate patches caused haemodynamic compensation and baroreflex resetting but no evidence of vascular reactivity tolerance. Novel NO donor drugs and delivery regimens which provide intermittent dosing may prevent the development of haemodynamic resetting rather than preventing vascular tolerance, a commonly perceived difficulty in chronic nitrate therapy.

show abstract

The contribution of vasopressin and angiotensin to the maintenance of blood pressure after autonomic blockade.

Cited by 27 publications

References 29 publications

Cardiovascular depression and stabilization by central vasopressin in rats.

Cardiovascular depression and stabilization by central vasopressin in rats.

Vascular amplifier properties in renovascular hypertension in conscious rabbits. Hindquarter responses to constrictor and dilator stimuli.

Baroreflex resetting but no vascular tolerance in response to transdermal glyceryl trinitrate in conscious rabbits

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