Hypertension: Multiple Membrane Malfunctions

Bohr, David F.; Harris, Andrea; Guthe, C C; Webb, R. Clinton

doi:10.1007/978-94-009-6741-0_10

Cited by 8 publications

(4 citation statements)

References 16 publications

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“…The time to half of maximal response for contraction in K+free solution was significantly shorter in carotid arteries from stroke-prone SHRs (51 f 2 minutes, n = 6) when compared with that in arteries from Wistar-Kyoto normotensive rats (70 f 2 minutes, n = 6, Fig. 4, 6 12 25 50 too…”

Section: Resultsmentioning

confidence: 89%

Calcium influx and vascular reactivity in systemic hypertension

Thompson

Bruner

Lamb

et al. 1987

The American Journal of Cardiology

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Numerous studies have focused on functional vascular changes that characterize the hypertensive state. Recent evidence that suggests that increased vascular reactivity in hypertension is due to changes in the delivery of activator Ca++ through channels in the cell membrane will be reviewed. The primary evidence supporting this hypothesis comes from studies that characterize the effects of Ca++-free solution and calcium channel blockers on contractile properties of isolated vascular smooth muscle. In the present study, experiments were performed to investigate the role of Ca++ influx in vascular contractions produced by interventions that cause membrane depolarization. Isometric tension development in helical strips of carotid arteries from stroke-prone spontaneously hypertensive rats in response to elevated K+ and tetraethylammonium chloride was greater than that in carotid arteries from Wistar-Kyoto normotensive rats. The rate of tension development to K+-free solution in carotid arteries from stroke-prone spontaneously hypertensive rats was faster than in Wistar-Kyoto normotensive rat arteries. Contractile responses to all 3 depolarizing interventions were reduced in arterial strips incubated in Ca++-free solution containing the chelator ethylene glycol bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid and in arterial strips treated with the Ca++ channel blocker verapamil. These results are consistent with the hypothesis that constrictor stimuli that produce membrane depolarization cause an opening of Ca++ channels in the plasma membrane that are sensitive to the organic channel blockers. Further, a change in Ca++ permeability or membrane depolarizing mechanisms contributes to increased contractile responsiveness in carotid arteries of stroke-prone spontaneously hypertensive rats.

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Section: Resultsmentioning

confidence: 89%

Calcium influx and vascular reactivity in systemic hypertension

Thompson

Bruner

Lamb

et al. 1987

The American Journal of Cardiology

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“…The extent to which vascular contractile re sponses depend on extracellular calcium concentration or are antagonized by calcium entry blockers has served as an index to com pare the calcium sensitivity of vascular smooth muscle from hypertensive and normotensive subjects. In general, contractile responses in blood vessels from hypertensive individuals are more sensitive to changes in extracellular calcium concentration [1][2][3] and to calcium entry blockers [4][5][6] than are those from normotensive individuals. These observations support the postulate that an alteration in the transmembrane movement of calcium contributes to increased vascular reactivity in hypertension.…”

Section: Introductionmentioning

confidence: 99%

Increased Vascular Reactivity to Bay K 8644 in Genetic Hypertension

1990

Pharmacology

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These experiments compared potential-operated calcium channel function in smooth muscle from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). Carotid artery strips from adult male SHRSP and WKY rats were suspended in tissue baths for isometric force recording. Contractile force was expressed as percent of response to 100 mmol/l KCl. Vascular strips from SHRSP were more sensitive to KCl (ED₅₀ = 25 mmol/l) compared to strips from WKY rats (ED₅₀ = 37 mmol/l). The calcium channel agonist Bay K 8644 (2.8 × 10^–10 to 2.8 × 10^–7 mol/l) produced tonic contractions in carotid artery strips from SHRSP (34% of the contractile response to 100 mmol/l KCl) but not in those from WKY rats. Incubation of vascular strips in 1.8 or 6 × 10^–10 mmol/l norepinephrine did not alter the maximal contractile response to Bay K 8644 in either strain of rats. In 12 mmol/l KCl, the maximal contractile response to Bay K 8644 was increased in both SHRSP (71%) and WKY rats (25%). In 18 mmol/l KCl, maximal contractile responses to Bay K 8644 in the two strains were similar (SHRSP = 73%, WKY = 76%). Removal of the endothelium did not significantly affect contractile responses to Bay K 8644 in either strain of rats. There were no differences in contractile responses to the calcium ionophore A23187 or in nifedipine-induced relaxation of potassium-activated vessels between carotid arteries from SHRSP and WKY rats. In summary, these results suggest that a difference in voltage-operated calcium channel function may underlie the increased sensitivity of SHRSP vascular smooth muscle to depolarizing stimuli.

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“…It seems likely that this mode of action is typical for asymmetrical cells with polar distribution of membrane trans¬ port systems. In contrast, in symmetrical cells like HML, the concordant movement of sodium and potassium is the result of events secondary to the increase in ic sodium owing to increased sodium permeability of the plasma membranes (Bohr et al 1984;Goodman 1981).…”

Section: Discussionmentioning

confidence: 96%

Effects of aldosterone on intralymphocytic sodium and potassium in patients with primary aldosteronism

Wehling¹,

Kuhls²,

Witzgall³

et al. 1987

Acta Endocrinologica

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In vitro effects of aldosterone have been described with regard to the intracellular sodium and potassium concentrations of human mononuclear leukocytes. In the present paper the in vitro effect of aldosterone on the intracellular sodium and potassium of human mononuclear leukocytes in 6 patients with primary aldosteronism was investigated. Except for one patient with elevated intracellular electrolytes, sodium and potassium in mononuclear leukocytes of patients with aldosteronism without incubation were within the range for normals. In the patients, no significant change of intracellular sodium or potassium was observed during incubation with or without aldosterone (1.4 nmol/l), whereas in normals, the loss of sodium and potassium during incubation without aldosterone was prevented by 1.4 nmol/l aldosterone. This insensitivity to aldosterone indicates that intracellular electrolytes in mononuclear leukocytes of patients with primary aldosteronism are kept in normal ranges by mechanism which are independent of mineralocorticoids and may represent the cellular correlate to the renal 'escape' phenomenon in aldosteronism.Recently, mineralocorticoid receptors and effects of aldosterone on intracellular (ic) sodium and potassium have been described for human mononuclear leukocytes (HML) (Armanini et al. 1985a;Wehling et al. 1987). The use of HML appears to provide an easily accessible model for studying the possible physiological effects of aldosterone bind¬ ing to type I receptors with regard to ic electro¬ lytes in vitro.The clinical significance of these receptors was underlined by the demonstration of absent or a decreased number of mineralocorticoid receptors and the lack of electrolyte response to aldosterone in HML of patients with pseudohypoaldosteronism (Armanini et al. 1985b; Wehlingetal. 1986).For patients with primary and secondary aldo¬ steronism, a reduced number of mineralocorti¬ coid receptors has been shown on HML (Armani¬ ni et al. 1987), thus indicating a 'down-regulation' in response to chronically elevated serum levels of aldosterone. It was hypothesized that this downregulation contributes to the 'escape' not only of HML, but also of renal tubular cells, from mine¬ ralocorticoid effects which opposes the develop¬ ment of more severe sodium retention and hypokalaemia in these patients. To further study the physiological implications of these findings at the cellular level, the miner¬ alocorticoid effector mechanism was investigated in HML of patients with primary aldosteronism. Patients and MethodsPatients Six patients with primary aldosteronism (4 males, 2 females; mean age ± SD 50.5 ± 7.6 years) were studied. Important clinical data and laboratory findings are summarized in Table 1. The diagnosis was suspected because of mild hypertension, mild hypokalaemia, elev-

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Hypertension: Multiple Membrane Malfunctions

Cited by 8 publications

References 16 publications

Calcium influx and vascular reactivity in systemic hypertension

Calcium influx and vascular reactivity in systemic hypertension

Increased Vascular Reactivity to Bay K 8644 in Genetic Hypertension

Effects of aldosterone on intralymphocytic sodium and potassium in patients with primary aldosteronism

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