The ionic composition of aortic smooth muscle from A.S.‐hypertensive rats

Massingham, R.; Shevde, S.

doi:10.1111/j.1476-5381.1973.tb08340.x

Cited by 13 publications

(4 citation statements)

References 8 publications

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“…They are consistent with the observations of others (32,33) in the spontaneously hypertensive rat and of Jones (34), who found alterations in ion kinetics rather than ion content with hypertension in rats. In blood vessels of other animal models of hypertension, there are increases in water, sodium, and potassium content in renal hypertension (35,36), in deoxycorticosterone hypertension (36), and in adrenal regeneration hypertension (37).…”

Section: Discussionsupporting

confidence: 93%

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Bevan¹,

Bevan²,

Chang³

et al. 1975

Circulation Research

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Vessel dimensions and characteristic responses to norepinephrine were measured in various arteries and veins of the rabbit made hypertensive by partial constriction of the upper abdominal aorta. The ear, radial, and basilar arteries taken from the circulation proximal to the ligature (the hypertensive arteries) were thickened in proportion to the rise in arterial blood pressure. The water, sodium, and potassium contents of these and all other vessels were not significantly changed in the hypertensive rabbits. The maximum response to norepinephrine in the ear artery, a representative vessel from the hypertensive part of the rabbit, was increased, whereas the sensitivity of this vessel to norepinephrine expressed as the ED 50 did not alter with changes in the arterial blood pressure. In contrast, the thickness and the maximum response to norepinephrine of the saphenous artery, representative of vessels distal to the ligature (normotensive vessels) and of the saphenous and cephalic veins were unaltered. The sensitivity as indicated by the norepinephrine ED 50 of the veins, but not of the saphenous artery, increased with a rise in carotid artery blood pressure. These results suggest that the increased responsiveness to norepinephrine of arteries proximal to the ligature is due to changes in muscle mass and that the increased responsiveness of the veins is due to increased sensitivity to norepinephrine.• The analysis of changes in responsiveness of blood vessels in hypertensive animal models has been the object of many investigations (1-14). A critical survey of these studies led us to define five experimental objectives, which served as the incentive for the present series of experiments. We wanted (1) to accurately determine the effect of hypertension on the responsiveness of vessels to norepinephrine in vitro using vessel rings; (2) to study a variety of vessels, including elastic and muscular arteries and veins, and (3) to separate local consequences of an increased intravascular pressure on the blood vessel wall from any generalized effects associated with the hypertensive state. We felt that (4) small early changes in the vessel wall should be observed if possible, since they are particularly relevant to the genesis of hypertension and that (5) control animal selection should minimize individual variation so that the small changes consequent to the hypertensive state could be recognized.The experimental model of hypertension which we chose to study was the rabbit with its abdominal aorta partially constricted between the celiac and anterior mesenteric arteries (15)(16)(17). In this preparation, after a few days the pressure in the arterial circulation proximal to the ligature becomes raised and that distal to the ligature returns to within the normal range. Although not all of our objectives were realized, many were satisfied by this approach. Existing techniques allowed measurements of vessel responsiveness to norepinephrine in both arteries and veins (18,19). A comparison of the changes in vessels tak...

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Section: Discussionsupporting

confidence: 93%

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Bevan¹,

Bevan²,

Chang³

et al. 1975

Circulation Research

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“…Numerous investigations have been done on arterial smooth muscle cells of the spontaneously hypertensive rat. In several studies an increased Ca2+ content of the arterial wall has been described [6,48,72], It remained open in these studies, whether intracellular or extracellu lar Ca2+ concentration was increased. Furthermore, there are also divergent reports on arterial Ca2+ content in spontaneously hypertensive rats [34].…”

Section: Spontaneously Hypertensive Ratsmentioning

confidence: 99%

Calcium and Primary Hypertension

Zidek

Vetter²

1987

Nephron

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The role of dietary calcium in essential hypertension remains controversial. Various studies have found on the one hand a weak negative correlation between blood pressure and Ca²⁺ intake in special groups, and on the other hand a positive correlation between serum Ca²⁺ concentration and blood pressure. Several disturbances of cellular Ca²⁺ metabolism have been described in essential hypertension and in the spontaneously hypertensive rat. Possibly the elevation of intracellular free Ca²⁺ concentration in arterial smooth muscle cells is one important step in the pathogenesis of primary hypertension. In most studies a decreased energy-dependent Ca²⁺ transport has been proposed as a mechanism. However, disturbances in cellular Ca²⁺ metabolism, which can be exclusively ascribed to essential hypertension, have not yet been found. The cause of altered cellular Ca²⁺ transport in primary hypertension may either be a genetically determined defect of membrane transport or a still unidentified humoral factor.

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“…In a series of experiments on SHR and normotensive controls Massingham and Shevde [11] measured a marked difference in the total calcium ion content of aortas from the two study groups. In this study, the hypertensive tissue contained approximately 65% more calcium than the normotensive tissue.…”

Section: Discussionmentioning

confidence: 99%

Age-dependent increase in arterial smooth muscle calcium in spontaneously hypertensive rats

et al. 1988

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Alterations in cellular calcium metabolism in essential hypertensive and in the SHR have been described. In the present study, particle-induced X-ray emission (PIXE) was used to get some information on the spatial distribution of Ca2+ in aortas of spontaneously hypertensive rats (SHR) and normotensive controls aged 1 week, 4 weeks, and 12 weeks. It was found that the Ca2+ content was not elevated in the aortic smooth muscle of SHR aged 1 week (n = 9) as compared to normotensive controls (n = 8) (186.8 +/- 89.9 micrograms Ca2+/g tissue vs 254.0 +/- 73.7 micrograms Ca2+/g tissue. The Ca2+ content was significantly raised in the aortic smooth muscle of SHR aged 4 weeks (n = 9) as compared to 4-weeks-old WKY rats (n = 12) (726.0 +/- 130.4 Ca2+/g tissue vs 440.3 +/- 214.4 Ca2+ micrograms/g tissue and in SHR aged 3 months (n = 15) as compared to WKY rats (n = 12), respectively (3317.0 +/- 734.0 micrograms Ca2+/g tissue vs. 1632.0 +/- 569.6 micrograms Ca2+/g tissue). The results confirm the age-related increase in the arterial Ca2+ content in normotensive rats and demonstrate additionally that this age-related rise in arterial Ca2+ content is accelerated in SHR.

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The ionic composition of aortic smooth muscle from A.S.‐hypertensive rats

Cited by 13 publications

References 8 publications

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Calcium and Primary Hypertension

Age-dependent increase in arterial smooth muscle calcium in spontaneously hypertensive rats

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