Mechanism of Renal Hypertension

Brown, J. J.; Davies, David; Morton, John J.; Robertson, James I.; Cuesta, V.; Lever, A.F.; Padfield, P. L.; Trust, P. M.; Bianchi, Giuseppe; Schalekamp, M. A. D. H.

doi:10.1016/s0140-6736(76)92165-6

Cited by 115 publications

(54 citation statements)

References 23 publications

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“…McGregor and Smirk," Finch, 12 and Collis and Alps 13 have shown the response of the mesenteric vasculature to All to be increased in renin-dependent renal hypertension. A normal or increased response in human renovascular hypertension has been described by Brown et al 14 The increased pressor response to All returned to normal after surgery. Bean et al 15 have shown an altered relation between arterial pressure and plasma All concentration after prolonged infusion of All in the dog, and Brown et al 16 have provided similar evidence in the rat.…”

Section: Discussionmentioning

confidence: 60%

Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats.

Schiffrin¹,

Thomé²,

Genest³

1983

Hypertension

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SUMMARY To determine the contribution of receptor number and affinity to changes in vascular reactivity to angiotensin II (AH) in hypertensive rats, we have investigated the binding of 125 I-AII to a participate fraction of the rat mesenteric artery of hypertensive rats. In two-kidney, one clip hypertensive rats, receptor concentration (Bmax) was 83 ± 13 fmol/mg and the dissociation constant (K d ) 0.6 ± 0 . 1 nM vs 75 ± 5.3 fmol/mg and 0.6 ± 0 . 1 nM«in normotensive controls, although PRA was much higher in the former. Bmax was reduced in these hypertensive rats after sodium depletion, as in normal rats. One-kidney, one clip hypertensive rats (Bmax 88 ± 17 fmol/mg, K d 0.6 ± 0 . 1 nM) did not differ from uninephrectomized control rats (96 ± 9 fmol/mg, K,, 0.5 ± 0.1 nM). In DOCA-salt hypertensive rats, binding capacity was increased (125 ± 2 fmol/mg, K,, 0.7 ± 0.0 nM) vs uninephrectomized salt-loaded rats (Bmax 95 ± 6 fmol/mg, K d 0.6 ± 0 . 1 nM), although PRA was suppressed comparably in both groups. The salt-loaded rats did not differ from uninephrectomized controls drinking water. We conclude that changes in the circulating renin-angiotensin system do not explain all the variations in receptor number in hypertensive rats. Our results suggest a role of mineralocorticoids in the regulation of vascular AH receptors.

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Section: Discussionmentioning

confidence: 60%

Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats.

Schiffrin¹,

Thomé²,

Genest³

1983

Hypertension

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“…2 In that animal model, during the first phase, which follows immediately upon unilateral renal artery constriction, the rise in blood pressure is explicable by the initial rise in renin and the direct pressor effect of the consequent elevation of plasma angiotensin II. 1 Within a few days, a second phase develops in which blood pressure remains high but plasma concentrations of renin and angiotensin II are proportionately lower.…”

Section: Discussionmentioning

confidence: 98%

Renal artery stenosis with normal angiotensin II values. Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery.

Atkinson¹,

Brown²,

Davies³

et al. 1981

Hypertension

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SUMMARYThe case is reported of a young woman with severe hypertension, unilateral renal artery stenosis, variously normal or marginally high plasma concentrations of active renin, angiotensin II, aldosterone, sodium, and potassium; and normal total exchangeable and total body sodium and potassium. Arteriograms and ureter catheterization showed the stenosis to be severe, but the unstimulated renal vein renin and angiotensin II differential to be modest. Captopril caused an initial fall in angiotensin II and arterial pressure. During prolonged captopril treatment, plasma angiotensin II and aldosterone remained depressed; exchangeable and total body sodium and potassium were unaltered. Blood pressure fell further to normal levels during prolonged captopril treatment, while subsequent surgical correction of the renal artery stenosis was curative; absolute values of blood pressure and plasma angiotensin II were similar in both situations.

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“…Consequently, aldosterone levels follow the same trend toward normalization (29,165). At this point in time, hypertension is almost entirely due to an increase in total peripheral resistance (20,29,84,137,165) and coexists with normal levels of cardiac output, circulating renin, angiotensin, and aldosterone (20,24,29,84,91). This pattern resembles all the characteristics of hypertension induced by slow responses to ANG II, including the transient elevation of circulating ANG II, and is also comparable to spontaneous hypertension in genetically inbred rats such as the salt-sensitive hypertension in Dahl rats.…”

Section: Renovascular Hypertensionmentioning

confidence: 93%

“…In the first phase, there is a very rapid increase of renal renin (131) and PRA (20,24,137,165), which generally correlates with the elevation of systemic blood pressure (Fig. 13) that lasts from 7 to 10 days (20,91,137).…”

Section: Renovascular Hypertensionmentioning

confidence: 97%

“…13) that lasts from 7 to 10 days (20,91,137). This first phase is also characterized by an increase in plasma aldosterone and certain volume retention, which may not be reflected in extracellular fluid volume expansion in a significant manner (20,24,165). After this phase, PRA comes down to near normal levels mainly due to the improvement of renal perfusion in the stenotic kidney because of hypertension.…”

Section: Renovascular Hypertensionmentioning

confidence: 99%

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Role of oxidative stress in angiotensin-induced hypertension

Reckelhoff

Romero

2003

American Journal of Physiology-Regulatory, Integrative and Comp

167

133

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Reckelhoff, Jane F., and J. Carlos Romero. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol Regul Integr Comp Physiol 284: R893-R912, 2003; 10.1152/ajpregu.00491.2002.-Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST.isoprostanes; endothelin; spontaneous hypertension; renovascular hypertension; sodium balance THREE DECADES AGO, the production of free radicals was thought to be the result of severe injuries or pathological insults such as those resulting from exposure to high-energy radiation or toxins such as carbon tetrachloride (127). However, in 1968, the discovery of superoxide dismutase (SOD) by McCord and Fridovich (96) strongly suggested that all aerobically metabolizing cells are capable of producing superoxide ions, which could play a role in normal metabolic processes. The concomitant discovery of the biology of nitric oxide (NO) strongly suggested that free radicals could constitute the basis of metabolic regulation (67,90,118). One of the first findings supporting such a notion was the demonstration that the inhibition of the synthesis of NO produced by the administration of an NO synthesis competitor, such as N -monomethyl-Larginine] or N G -nitro-L-arginine methyl ester (L-NAME), produced a marked vasoconstriction (13,136,173), sodium retention (82, 83), and thereby a sustained increase in mean arterial pressure (MAP) (13,82,83,136,173). The identification of a specific pathological situation in humans, where a decrease of NO may end up in an elevation of blood pressure was thought to be linked to endothelial dysfunction (105), such as those involved in aging, arteriosclerosis, etc., but the specific metabolic alterations involved in this process were poorly understood. However, the relationship betw...

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Mechanism of Renal Hypertension

Cited by 115 publications

References 23 publications

Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats.

Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats.

Renal artery stenosis with normal angiotensin II values. Relationship between angiotensin II and body sodium and potassium on correction of hypertension by captopril and subsequent surgery.

Role of oxidative stress in angiotensin-induced hypertension

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