Central and Peripheral Noradrenaline in the Two Kidney Model of Renovascular Hypertension in the Rat

Dargie, H. J.; Franklin, Stanley S.; Reid, John L.

doi:10.1111/j.1476-5381.1977.tb08406.x

Cited by 21 publications

(6 citation statements)

References 10 publications

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“…In contrast with these reports, we found potentiation of pressor responses to 0.9 and 3.0 nmol of NA in MAB from obese rats by a concentration of insulin (200 mU/L) close to that the obese rats are exposed to in vivo. This suggests that exposure to chronic hyperinsulinemia enhances vascular reactivity to concentrations of NA that are within the physiological range for circulating NA in rats (Dargie et al 1977;Katholi et al 1982). Thus, hyperinsulinemia may be physiologically relevant in promoting hypertension in obese Zucker rats.…”

Section: Discussionmentioning

confidence: 86%

Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin

He¹,

MacLeod²

2002

Can. J. Physiol. Pharmacol.

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The genetically obese Zucker rat (fa/fa) is an insulin-resistant animal model with early-onset severe hyperinsulinemia that eventually develops mild hypertension. Thus, it represents a model in which the effect of hyperinsulinemia - insulin resistance associated with hypertension on vascular reactivity can be examined. The purpose of this study was to investigate the contribution of endogenous nitric oxide (NO) and prostaglandins to reactivity to noradrenaline (NA) in the presence and absence of insulin in mesenteric arterial beds (MAB) from 25-week-old obese Zucker rats and their lean, gender-matched littermates. In the absence of insulin, bolus injection of NA (0.9-90 nmol) produced a dose-dependent increase in perfusion pressure in MAB from both lean and obese rats. Although there was no significant difference in NA pD2 (-log ED50) values, the maximum response of MAB from obese rats to NA was slightly but significantly reduced compared with that of MAB from lean rats. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 300 microM) enhanced and indomethacin (20 microM) inhibited pressor responses to NA in MAB from both obese and lean rats. Perfusion with insulin (200 mU/L, a level similar to that in obese rats in vivo) potentiated only the responses of the obese MAB to the two lowest doses of NA tested (0.9 and 3 nmol). In the presence of L-NMMA, insulin further potentiated the NA response in MAB from obese rats. Indomethacin, the prostaglandin H2/thromboxane A2 receptor antagonist SQ 29548 (0.3 microM), and the nonselective endothelin-1 (ET-1) receptor antagonist bosentan (3 microM) all abolished insulin potentiation of the NA response in obese MAB. These data suggest that concurrent release of NO and vasoconstrictor cyclooxygenase product(s) in MAB from both obese and lean Zucker rats normally regulates NA-induced vasoconstrictor responses. Furthermore, insulin increases the release of contracting cyclooxygenase product(s) and enhances reactivity to low doses of NA in MAB from obese rats. The effects of insulin may be partially mediated by ET-1 via ET receptors and are buffered to some extent by concomitant NO release. This altered action of insulin may play a role in hypertension in this hyperinsulinemic - insulin-resistant model.

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Section: Discussionmentioning

confidence: 86%

Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin

He¹,

MacLeod²

2002

Can. J. Physiol. Pharmacol.

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“…Our evidence of increased sympathetic tone in this form of hypertension is not in agreement with the absence of a sympathetic component in the 2K-1C Goldblatt hypertensive rat noted in another study. 17 The contribution of the sympathetic nervous system to the hypertension in our dogs may, in fact, have been underestimated. The mean 75% depletion achieved with the 5 mg/kg dose of guanethidine that we employed may not have produced maximal inhibition of sympathetic tone.…”

Section: Discussionmentioning

confidence: 89%

“…When 6-hydroxydopamine was given intracisternally in doses of 250 jig two to three times before clamping, it prevented 1K-1C Goldblatt hypertension from developing, 10 but had no effect on 2K-1C hypertension. 17 When administered systemically, 6-hydroxydopamine combined with adrenal medullectomy inhibited the development of 2K-1C hypertension in adult and weanling rats, 18 but only delayed the full complement of 1K-1C hypertension. 19 Large-dose guanethidine treatment of newborn rats, not combined with adrenalectomy, failed to alter the development of 1K-1C or 2K-1C hypertension."…”

mentioning

confidence: 98%

“…Based on the ability of 6-hydroxydopamine given intracisternally to prevent induction of 1K-1C, but not 2K-1C, Goldblatt hypertension, and the finding of an increased plasma catecholamine level in the former but not latter model, it was concluded that neither the central nor peripheral sympathetic nervous system participates in 2K-1C Goldblatt hypertension in the rat. 17 ' » Because of previous suggestions in the literature for sympathetic involvement in 2K-1C Goldblatt hypertension, 18 ' 23 and the known interactions of angiotensin with both central 24 and peripheral components of the sympathetic nervous system, 25 we initiated this investigation. We wished to determine the influence of the sympathetic and renin-angiotensin systems on the blood pressure and renal blood flow in the 2K-1C Goldblatt hypertensive dog.…”

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confidence: 99%

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Sympathetic and renin-angiotensin system influence on blood pressure and renal blood flow of two-kidney, one clip Goldblatt hypertensive dog.

Zimmerman¹,

Mommsen²,

Kraft³

1980

Hypertension

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“…Normal plasma catecholamine levels found in two-kidney, one-clip hypertensive rats do not exclude the possibility of adrenergic participation in regulating renovascular resistances. Both increased (Grewal & Kaul, 1971) and decreased (Dargie, Franklin & Reid, 1977) sympathetic tone in this form of hypertension have been reported.…”

Section: Discussionmentioning

confidence: 99%

Renal Haemodynamics in Conscious Experimentally Hypertensive Rats

Charocopos

1983

Exp Physiol

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SUMMARYThe integrity of renal haemodynamics is essential for the maintenance of normal renal function in the normotensive and hypertensive state. Systemic and renal haemodynamics have been determined by the radioactively labelled microspheres technique in normotensive, Goldblatt I, Goldblatt II and deoxycorticosterone (DOC)-saline-treated hypertensive rats. Cardiac output was similar between normotensive and hypertensive rats, while total peripheral resistance was similarly higher in all hypertensive animals when compared to normotensive animals. Renal blood flow per weight unit was similarly decreased in all hypertensive animals (3 77 ml/min . g (S.D. 0-85, n = I 1); the unclipped kidneys of Goldblatt II rats, 3 76 ml/min . g (S.D. 0 89, n = I 1); the clipped kidneys of Goldblatt II rats, 3 62 ml/min. g (S.D. 078, n = 9); the kidneys of Goldblatt I rats and 2 95 ml/min . g (S.D. 0 83, n = 10) the kidneys of DOC-saline rats). It is concluded that kidneys from experimentally hypertensive rats fail to preserve normal renal blood flow, even at elevated arterial blood pressures, regardless of the pathophysiology of hypertension.

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Central and Peripheral Noradrenaline in the Two Kidney Model of Renovascular Hypertension in the Rat

Cited by 21 publications

References 10 publications

Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin

Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin

Sympathetic and renin-angiotensin system influence on blood pressure and renal blood flow of two-kidney, one clip Goldblatt hypertensive dog.

Renal Haemodynamics in Conscious Experimentally Hypertensive Rats

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