Neural and local control of arterioles in SHR.

Lombard, Julian H.; Hess, Marilyn E.; Stekiel, William J.

doi:10.1161/01.hyp.6.4.530

Cited by 44 publications

(28 citation statements)

References 21 publications

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“…The greater constriction of arterioles of hypertensive rats in response to increased oxygen availability is consistent with previous studies of spontaneously hypertensive rats in the early 14 and established stages of hypertension, and rats with one-kidney, one clip renal hypertension. 33 An increase in the oxygen content of the superfusion solution results in an increase in tissue P02 and periarteriolar Po?.…”

Section: Microcirculatory Studiessupporting

confidence: 90%

Hemodynamics and microcirculatory alterations in reduced renal mass hypertension.

1989

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The objectives of this study were to determine the hemodynamic and microcirculatory changes that occur during reduced renal mass hypertension in rats. In conscious animals with 75% reduction of total renal mass, mean arterial pressure was initially (4-8 hours) elevated by 15-20 mm Hg during intravenous infusion with isonatremic (145.4 mM) NaCl. Cardiac index was elevated by 15-20%, and total peripheral resistance index was normal or reduced. Cardiac index subsequently returned toward normal, but mean arterial pressure remained elevated (20-40 mm Hg), presumably because of an elevated total peripheral resistance. Cremasteric arterioles were actively constricted (35-50%) in rats with short-term (36 hours), but not chronic (5-6 weeks) reduced renal mass hypertension. Total microvessel density was approximately 15% lower in maximally dilated cremaster muscles of chronically hypertensive rats versus sham-operated controls, which suggests that arterioles are lost during sustained reduced renal mass hypertension. Arteriolar constriction in response to increased superfusate Po? (0% to 5% O*) was 2 -4 times greater in rats with both short-term and chronic reduced renal mass hypertension than in normotensive controls, which suggests that oxygen-dependent autoregulatory mechanisms are altered. The hemodynamic and microcirculatory alterations observed in these experiments suggest that classic short-term autoregulatory mechanisms and an enhanced response of arterioles to increased oxygen availability contribute to the elevated total peripheral resistance in short-term reduced renal mass hypertension, whereas structural changes and altered vascular oxygen responses contribute to an elevated microvascular resistance in chronic reduced renal mass hypertension. {Hypertension 1989;13:128-138)

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Section: Microcirculatory Studiessupporting

confidence: 90%

Hemodynamics and microcirculatory alterations in reduced renal mass hypertension.

1989

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“…4 All other groups of rats had normal blood pressures. Heart rates were higher in rats on a high salt diet than the respective control rats on a low salt diet although an elevation in blood pressure did not occur in some of these groups.…”

Section: Hemodynamic Parametersmentioning

confidence: 90%

“…{Hypertension 1990;15:779-783) C onsiderable evidence has been accumulated to indicate that both changes in vessel caliber and vessel number can contribute to the increased vascular resistance in hypertension. 1 - 4 The degree to which variations in microvessel density alone contribute to the increase in total peripheral resistance in hypertension has been debated. 10 In most of these studies, microvessel density has been estimated either from intravital measurements or from injection methods.…”

Section: Microvessel Changes In Hypertension Measured By Griffonia Simentioning

confidence: 99%

Microvessel changes in hypertension measured by Griffonia simplicifolia I lectin.

et al. 1990

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Commonly used methods for assessing reductions in microvascular density (rarefaction) in hypertension detect only perfused microvessels. In the present study, samples of cremaster and spinotrapezius muscles were taken from rats with chronic (4-week) reduced renal mass hypertension and normotensive sham-operated control rats, as well as from 12-week-old spontaneously hypertensive rats and their normotensive Wistar-Kyoto control strain. Mean arterial pressure was 149±8 mm Hg in the rats with reduced renal mass hypertension, 114±7 mm Hg in sham-operated rats, 177±9 mm Hg in spontaneously hypertensive rats, and 95±4 mm Hg in Wistar-Kyoto rats. Muscle samples were incubated with rhodamine-labeled Griffonia simplicifolia I lectin, which identifies both perfused and nonperfused microvessels. Microvascular density was assessed by counting intersections with a 20-/um grid. Microvessel density was significantly reduced in cremaster muscles of both spontaneously hypertensive and reduced renal mass hypertensive rats, and in the spinotrapezius muscle of spontaneously hypertensive rats, compared with their respective normotensive controls. Further studies in the reduced renal mass rats on low salt diets indicated that lectin binding was also decreased as salt intake was increased, independent of blood pressure. This change was not due to an alteration in lectin-binding affinity. These studies indicate that lectin binding can be a useful tool for assessing microvessel density that does not depend on the perfusion state of the vessels and that rarefaction due to hypertension is not evenly distributed in all vascular beds. These results also provide evidence that dietary salt intake alone can influence microvessel density, as measured by the lectin technique. {Hypertension 1990;15:779-783) C onsiderable evidence has been accumulated to indicate that both changes in vessel caliber and vessel number can contribute to the increased vascular resistance in hypertension.

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“…Studies on cremaster muscle provided evidence for elevation of arteriolar tone in SHR after vasodilation with adenosine. 9 '" Lombard et al 9 also found the greatest dilation in the region of the third-order (A3) arterioles (which are close to the transverse arterioles in our terminology) and attributed the effect to a higher neural transmission and more vigorous responses to oxygen. These observations are compatible with the greater density of nerve plexes in arterioles of SHR 20 and an elevated central sympathetic nerve activity.…”

Section: Previous Studiesmentioning

confidence: 51%

“…9 ' l0 Thus, the present study attempted to ascertain the degree of smooth muscle contraction along arteriolar pathways in the spinotrapezius muscle of SHR and their normotensive controls, the WKY, under normal perfusion conditions.…”

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confidence: 99%

Microvascular tone in a skeletal muscle of spontaneously hypertensive rats.

Schmid‐Schönbein

Zweifach²,

DeLano³

et al. 1987

Hypertension

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SUMMARY We studied the degree of arteriolar smooth muscle constriction in the spinotrapezius muscle microcirculation of spontaneously hypertensive rats and their normotensive controls, WistarKyoto rats. The constriction was expressed in the form of a nondimensional tone as the difference between steady state and dilated diameter (after papaverine treatment) divided by the dilated diameter. Both animal strains showed on average a progressive increase of tone toward the more distal arterioles, with a peak tone being reached in the transverse arterioles. Tone values in the hypertensive animals were consistently elevated. The number of arterioles that had more than 5% tone (so-called responder arterioles) was higher in the hypertensive animals. These studies suggest that, besides the anatomical adjustments documented earlier in our laboratory in the arteriolar network of this muscle, functional adjustments in the form of an elevated microvascular tone are associated with the elevated resistance in spontaneously hypertensive rats. (Hypertension 9: 164-171, 1987) KEY WORDS • tone skeletal muscle arteriole • spontaneous hypertension • microcirculation O UR earlier studies of the microcirculation dealing with the spontaneous form of hypertension in rats 1 showed that resistance is increased across the hierarchy of precapillary arterioles, as evidenced by the altered pressure-flow relationships in consecutive segments of the spinotrapezius muscle bed. There are, however, insufficient data concerning the factors responsible for such alterations. Previous workers advanced the so-called rarefaction concept of hypertension 2 when they found that there was no statistically significant decrease in the diameter of comparable arterioles in order to account for the above-normal microvascular resistances in spontaneously hypertensive rats (SHR). Experimental data in support of arteriolar rarefaction have been advanced for the cremaster 2 and anterior gracilis muscle preparations 3 of SHR and for the renal form of hypertension. 4 Few of the studies in the literature have estimated microvascular resistance levels on the basis of direct measurements of pressure and flow in the various sections of the network. Our own studies of the problem in

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Neural and local control of arterioles in SHR.

Cited by 44 publications

References 21 publications

Hemodynamics and microcirculatory alterations in reduced renal mass hypertension.

Hemodynamics and microcirculatory alterations in reduced renal mass hypertension.

Microvessel changes in hypertension measured by Griffonia simplicifolia I lectin.

Microvascular tone in a skeletal muscle of spontaneously hypertensive rats.

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