The Question of Vascular Hyper-Responsiveness in Hypertension

Redleaf, Paul D.; Tobian, Louis

doi:10.1161/01.res.6.2.185

Cited by 72 publications

(19 citation statements)

References 12 publications

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“…Their increased sensitivity to angiotensin is similar to that noted for various pressor substances (19) and may be related to the decreased size of the vascular lumen (20) or the higher initial blood pressure (21).…”

Section: Discussionsupporting

confidence: 73%

The Effect of Angiotensin II on the Blood Pressure in Humans with Hypertensive Disease*

Kaplan¹,

Silah²

1964

J. Clin. Invest.

267

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Section: Discussionsupporting

confidence: 73%

The Effect of Angiotensin II on the Blood Pressure in Humans with Hypertensive Disease*

Kaplan¹,

Silah²

1964

J. Clin. Invest.

267

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“…During the course of this study, the results of a similar investigation were published by Redleaf and Tobian. 10 These authors found that the aortas of their hypertensive animals responded, in most instances, to epinephrine, in the same way as did the aortas of their normotensive controls, a few responding with even decreased reactivity. We have found that if aortic hypertrophy is taken into consideration, and conditions of comparison carefully controlled, the development of DCAsalt hypertension in rats is almost always, and renal hypertension often, associated with decreased rather than increased contractile responses of aortic smooth muscle to epinephrine and levarterenol.…”

mentioning

confidence: 92%

Comparative Reactivities of Aortic Strips from Hypertensive and Normotensive Rats to Epinephrine and Levarterenol

Mallov

1959

Circulation Research

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Rats were rendered hypertensive by two different technics. Isometric tensions developed by strips of aorta from these rats, when exposed to various concentrations of epinephrine and levarterenol, were compared with those developed by aortic strips from normotensive controls. Almost all of the aortic strips from the DCA-salt hypertensive rats responded with smaller contraction tensions to both pressor agents than did the corresponding control strips from the normotensive animals. The same was true for most of the strips obtained from the renal hypertensive rats. These results do not lend support to the hypothesis that vascular hyperreactivity is the basis of many forms of hypertension.T SE SUGGESTION has appeared in the literature, from time to time, that the increased arteriolar resistance present in essential hypertension may be due to an enhanced sensitivity of the vascular smooth muscle to pressor agents normally found in the circulation or released by nerve endings. A number of studies of human hypertensives, and also of animals rendered hypertensive by experimental means, have yielded data tending to support such a hypothesis. """ The work presented in this paper was done in order to determine whether the development of experimental hypertension in animals is indeed associated with an increased vascular reactivity. It was considered advisable to study vascular strips in vitro, so that circulatory, nervous, and similar influences present in the whole animal could be eliminated. Aortic smooth muscle was chosen for convenience, with the realization that the responses of aortic and arteriolar smooth muscle to diugs may not necessarily be alike. During the course of this study, the results of a similar investigation were published by Redleaf and Tobian. 10These authors found that the aortas of their hypertensive animals responded, in most instances, to epinephrine, in the same way as did the aortas of their normotensive controls, a few responding with even decreased reactivity. We have Supported by a grant from the American Heart Association.Received for publication September 29, 1958. found that if aortic hypertrophy is taken into consideration, and conditions of comparison carefully controlled, the development of DCAsalt hypertension in rats is almost always, and renal hypertension often, associated with decreased rather than increased contractile responses of aortic smooth muscle to epinephrine and levarterenol. METHODSMale albino ruts of the Wistar strain were rendered hypertensive by two different procedures. In the first, rats weighing 80 to 100 Gm. at the start were injected intramuscularly at weekly intervals with 5 ing. of desoxycorticosterone trimethylacetate, 5 and given 1 per cent NaCl in place of drinking water. They were fed Purina laboratory chow ad libitum. Control rats receiving no special treatment were maintained on Purina chow and water ad libitum. The animals were killed in pairs (1 normotensive control and 1 hypertensive rat) after various intervals of time ranging from 14 to So days. In...

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“…Thus, abnormalities observed could such "waterlogging" of arterial walls increases vascular resistance and responses. 2 tension of structural changes increasing vascular wallto-lumen ratio. 4 It is especially important to determine if such structural changes occur in resistance vessels in hypertension in the absence of increases in intravascular pressure.…”

mentioning

confidence: 98%

Increased resistance and impaired maximal vasodilation in normotensive vascular beds of rats with coarctation hypertension.

Bell¹,

Overbeck²

1979

Hypertension

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SUMMARY To study the resistance of normotensive vascular beds in coarctation hypertension, we measured perfusion pressures of pump-perfused (blood), innervated, isolated hindlimbs of 12 rats (Group A) with 4 weeks of hypertension due to partial constriction of the abdominal aorta above the renal arteries, and of three control groups: 11 normotensive rats (Group B) with aorta sham-constricted, nine normotensive rats (Group C) with slight (5%) hindquarters atrophy due to partial constriction of the abdominal aorta below the renal arteries, and six rats with two-kidney, one clip Goldblatt hypertension (Group D). After aortic constriction, measured femoral arterial pressures in Group A rats remained normotensive. In hypertensive rats of Groups A and D, compared to normotensive Group B or C rats, hindlimb pressure-flow curves were displaced toward the pressure axis (p < 0.05). Compared to normotensive rats, drop in hindlimb resistance after acute local nerve section was increased in rats with coarctation hypertension. Residual resistance after maximal vasodilation with intraarterial sodium nitroprusside remained elevated in hypertensive rats of Groups A and D (p < 0.05), as compared to normotensive Group B or C rats; compared to Group B rats, this residual resistance in the coarcted rats of Group A was increased by 9%. Thus, in normotensive vascular beds of rats with chronic hypertension caused by aortic coarctation, resistance is elevated. The neurogenic component contributes to this high resistance, and structural vascular changes, indicated by impaired maximal vasodilation, may also contribute to the elevated resistance. It is most unlikely that these resistance changes are attributable to elevated hindlimb intravascular pressures. (Hypertension 1: 78-85, 1979 not be said to be merely secondary to increased intramodel for examining the effects of intravasvascular pressure. We have previously reported incular pressure on vascular structure and creased salt and water content in the walls of arteries function in hypertension, because the vascular beds from these normotensive vascular beds in rats with below the coarctation are not exposed to elevated coarctation hypertension. 1 It has been suggested that levels of pressure. Thus, abnormalities observed could such "waterlogging" of arterial walls increases vascular resistance and responses.

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The Question of Vascular Hyper-Responsiveness in Hypertension

Cited by 72 publications

References 12 publications

The Effect of Angiotensin II on the Blood Pressure in Humans with Hypertensive Disease*

The Effect of Angiotensin II on the Blood Pressure in Humans with Hypertensive Disease*

Comparative Reactivities of Aortic Strips from Hypertensive and Normotensive Rats to Epinephrine and Levarterenol

Increased resistance and impaired maximal vasodilation in normotensive vascular beds of rats with coarctation hypertension.

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