α1-Adrenergic receptors in cardiac ventricles of dahl rats

Hayashi, Shûichi; Umemura, Satoshi; Ashino, Kazuhiro; Hirawa, Nobuhito; Toya, Yoshiyuki; Abe, Yasuhiko; Ishii, Masao

doi:10.1016/0895-7061(95)00142-c

Cited by 4 publications

(3 citation statements)

References 18 publications

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“…37 Further, the maximal binding of ␣ 1 -adrenoreceptors in cardiac ventricles has been found to be greater in male than in female Dahl rats. 38 Interestingly, these authors observed that there was a greater variability in maximal binding in the female rats that may have been related to the estrous cycle. Our data demonstrate a novel role of estradiol on ␣ 1 -adrenergic expression.…”

Section: Zhang and Davidge Estrogen Replacement And Vascular Reactivitymentioning

confidence: 96%

Effect of Estrogen Replacement on Vasoconstrictor Responses in Rat Mesenteric Arteries

Zhang

Davidge

1999

Hypertension

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Abstract-Recent studies have shown that estrogen can increase endothelial nitric oxide synthase expression and/or activity and that nitric oxide may play a role in attenuating vasoconstrictor responses. Yet there are still controversies in this field. Our hypothesis was that the role of nitric oxide in modulating vasoconstrictor responses in estrogen-replaced animals depends on the agonist. The aim of the study was to determine the effect of long-term estrogen replacement on vascular reactivity of resistance-sized mesenteric arteries in ovariectomized rats with the use of a variety of vasoconstrictors. Female Sprague-Dawley rats were ovariectomized at 11 weeks of age. 17␤-estradiol pellets (0.5 mg/pellet) were implanted in the estrogen-replaced group (nϭ9) for 4 weeks; placebo pellets were used in the ovariectomized group (nϭ10). Resistance-sized mesenteric arteries were dissected and mounted onto a dual-chamber arteriograph system. Estradiol replacement did not alter the response of mesenteric arteries to either arginine vasopressin or the thromboxane mimetic U46619. Inhibition of nitric oxide synthase with N G -monomethyl-L-arginine (100 mol/L) did not modulate these vasoconstrictor responses in either group of rats. In contrast, the dose-response curve of the adrenergic agonist phenylephrine was significantly attenuated for the estradiol-replaced rats compared with the ovariectomized group (EC 50 ϭ0.90Ϯ0.17 vs 0.44Ϯ0.08 mol/L, PϽ0.05). After incubation with N G -monomethyl-Larginine, the EC 50 of phenylephrine significantly decreased in both groups, but a significant difference remained between the 2 groups (EC 50 ϭ0.41Ϯ0.08 vs 0.28Ϯ0.02 mol/L, PϽ0.05). Importantly, Western immunoblotting demonstrated that the expression of ␣ 1 -adrenergic receptors was significantly suppressed by estradiol replacement. We conclude that estrogen may have a specific effect on adrenergic vasoconstriction by modulating its receptors. (Hypertension. 1999;34:1117-1122.) Key Words: steroids Ⅲ nitric oxide Ⅲ receptors, adrenergic, alpha Ⅲ vasopressin Ⅲ thromboxanes E pidemiological studies have shown that the incidence of cardiovascular disease in premenopausal women is lower than that in men and postmenopausal women. 1,2 This is believed to be due to the protective effect of circulating estrogen because estrogen replacement therapy significantly reduces the incidence of cardiovascular disorders in postmenopausal women. 3,4 The vascular wall has been shown to contain specific high-affinity receptors for estrogen both in humans 5,6 and in animals, 7-9 providing strong biological evidence that the cardiovascular system is one of the targets of estrogen. However, the exact mechanisms of the protective effect of estrogen are still unknown.Estrogen treatment in animal models increases systemic and uterine blood flow 10 -13 and attenuates the pressor response to phenylephrine (PE) in mesenteric 14 and aortic arteries. 15 Many of these studies have implicated nitric oxide (NO) as the mediator of the altered vascular response resulting from...

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Section: Zhang and Davidge Estrogen Replacement And Vascular Reactivitymentioning

confidence: 96%

Effect of Estrogen Replacement on Vasoconstrictor Responses in Rat Mesenteric Arteries

Zhang

Davidge

1999

Hypertension

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“…An elevated density of renal α 2 -adrenergic receptors was found in spontaneously hypertensive rats (SHR), in Dahl salt-sensitive (DS) and in Sabra strain (SBH). In these animals, both heart weight and receptor density were increased, suggesting the possible involvement of α 1 -adrenoceptors in cardiac hypertrophy (28). Animal models of acquired hypertension have unchanged or decreased renal α 2adrenergic receptors.…”

Section: Peripheral Adrenergic System and Hypertensionmentioning

confidence: 87%

Peripheral Adrenergic System and Hypertension

Veglio¹,

Cella²,

Schiavone³

et al. 2001

Clinical and Experimental Hypertension

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Hypertension is a condition where adrenergic responsiveness, sympathetic activity and adrenoceptors are somewhat altered. Many techniques are available to assess human sympathetic nervous system activity. They each present limitations and disadvantages. Characterization and subdivision of the alpha and beta-adrenoceptors, according to their localization and answer to different agonists, was facilitated in recent years by the extensive use of pharmacological and molecular biology techniques. Some adrenoceptor studies were conducted on animal models, human tissues and peripheral blood cells to assess their changes in various forms and stages of hypertension. Our group has pointed out that alpha1-adrenergic receptors expressed by human peripheral blood lymphocytes underwent changes of density in essential hypertensives, compared to normotensive control subjects. The importance of these findings could provide an assessment of alpha1-peripheral receptors with possible future clinical implications in the pathophysiology and treatment of hypertension.

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“…At 6, 8 and 10 weeks of age, systolic blood pressure (SBP) and bodyweight were measured. Systolic blood pressure was measured by tail‐cuff plethysmography, as described previously 19 . After rats were killed at 10 weeks of age by decapitation, their hearts were rapidly excised, washed in cold saline, separated into ventricles and atria and weighed.…”

Section: Methodsmentioning

confidence: 99%

Angiotensin Ii Receptors in Cardiac Left Ventricles of Dahl Rats

Sumida

Umemura

Kobayashi

et al. 1998

Clin Exp Pharma Physio

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1. Dahl Iwai salt-sensitive (DS) rats have been reported as becoming hypertensive with left ventricular hypertrophy (LVH) and heart failure when on a high-salt diet. Their circulating renin-angiotensin system (RAS) has been reported to be suppressed. To evaluate the role of angiotensin II (AngII) type 1 and type 2 receptors (AT1 and AT2, respectively) in LVH, we compared cardiac AT1 and AT2 receptors in 10-week-old DS rats and Dahl Iwai salt-resistant (DR) rats. 2. Seven pairs of 6-week-old male DS and DR rats were fed either a low- or high-salt diet (0.3 or 8% NaCl, respectively) for 4 weeks. Left ventricular AngII receptors were measured by radioligand binding assays using [125I]-[Sar1,Ile8]-AngII in plasma membrane fractions from these four groups. The AT1 and AT2 receptors were distinguished using their specific antagonists CV 11974 and PD 123319, respectively. 3. The high-salt diet increased blood pressure and the left ventricle:bodyweight ratio in DS rats. However, neither Bmax for AT1 and AT2 receptors nor Kd for [125I]-[Sar1,Ile8]-AngII differed between the groups. These results are different from those of other reports of pressure-overload LVH, such as spontaneously hypertensive rats or renovascular hypertension rats, in which AT1 and AT2 receptors were reported to be up-regulated.

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α1-Adrenergic receptors in cardiac ventricles of dahl rats

Cited by 4 publications

References 18 publications

Effect of Estrogen Replacement on Vasoconstrictor Responses in Rat Mesenteric Arteries

Effect of Estrogen Replacement on Vasoconstrictor Responses in Rat Mesenteric Arteries

Peripheral Adrenergic System and Hypertension

Angiotensin Ii Receptors in Cardiac Left Ventricles of Dahl Rats

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