Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats.

Smith, Jacquelyn M.; Jones, Allan W.

doi:10.1161/01.hyp.15.1.78

Cited by 21 publications

(18 citation statements)

References 31 publications

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“…The finding that nifedipine reduced the basal 86Rb efflux rate constant only in SHR arteries clearly indicates that extracellular Ca2" enters the cell via L-type voltage-dependent Ca2" channels in the resting state of SHR arteries, activates Kca channels, and thus contributes to the increased K+ permeability. Similar results were reported for the resting state of the aorta from aldosterone-salt hypertensive rats in which the effects of calcium channel blockers on basal tension and the elevated 42K efflux were evaluated (Smith & Jones, 1990). Judging from the effect of nifedipine Figure 6, the contribution of the Ca2" influx to the increased K+ permeability was greater in carotid and femoral arteries than in mesenteric arteries.…”

Section: Discussionsupporting

confidence: 75%

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Asano

Masuzawa-Ito

Matsuda

1993

British J Pharmacology

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1 To determine the possible role of Ca2"-activated K+ (Kca) channels in the regulation of resting tone of arteries from spontaneously hypertensive rats (SHR), the effects of agents which interact with these channels on tension and 16Rb efflux were compared in endothelium-denuded strips of carotid, femoral and mesenteric arteries from SHR and normotensive Wistar-Kyoto rats (WKY). 2 Strips of carotid, femoral and mesenteric arteries from SHR exhibited a myogenic tone; that is, the resting tone decreased when either the Krebs solution was changed to a 0-Ca2+ solution or 10-7M nifedipine was added.3 The addition of charybdotoxin (ChTX, I0-'-I0-M), a blocker of large conductance Kca channels, to the resting strips of these arteries produced a concentration-dependent contraction, which was significantly greater in SHR than in WKY. Relatively low concentrations of tetraethylammonium (0.05-5 mM) produced a concentration-dependent contraction which was similar to the ChTX-induced contraction in these strips. 4 The ChTX-induced contractions in SHR were greatly attenuated by 10-7 M nifedipine and by 3 X 10-6 M cromakalim, a K+ channel opener. Cromakalim alone abolished the myogenic tone in SHR. 5 The addition of apamin (a blocker of small conductance Kca channels, up to 10-6 M), or of glibenclamide (a blocker of ATP-sensitive K+ channels, up to 5 x 10-6 M ), to the resting strips failed to produce a contraction.6 In resting strips of carotid, femoral and mesenteric arteries preloaded with 86Rb, the basal 86Rb efflux rate constants were significantly greater in SHR than in WKY. The addition of 10-7 M nifedipine to the resting strips decreased the basal 86Rb efflux rate constants only in SHR. 7 The cellular Ca2+ uptake in the resting state of carotid and femoral arteries from SHR was significantly increased when compared to WKY, and this increase in SHR was significantly reduced by 10-7 M nifedipine. 8 These results suggest that the ChTX-sensitive KCa channels were highly activated to regulate the myogenic tone in the resting state of carotid, femoral and mesenteric arteries from SHR. The increased Kca channel functions in SHR arteries appeared to be secondary to the increased Ca2' influx via L-type voltage-dependent Ca2+ channels in the resting state of these arteries.

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Section: Discussionsupporting

confidence: 75%

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Asano

Masuzawa-Ito

Matsuda

1993

British J Pharmacology

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“…We hold this view based on previous studies both from our laboratory and those of others demonstrating virtually no influence on arterial hypertension of diets differing widely in sodium content (14,24,25). Vascular actions of aldosterone, for example, to enhance ion permeability in vascular smooth muscle, to reset baroreceptors, or to amplify local vasoconstrictor systems likely ally in the hypertensive action of aldosterone both in the remnant kidney and the mineralocorticoid/salt model (26)(27)(28)(29). Glomerular capillary pressures were not measured but we suspect are elevated in the aldosterone supplementation since they are clearly increased in the mineralocorticoid salt model of hypertension (30).…”

Section: Discussionmentioning

confidence: 83%

Role of aldosterone in the remnant kidney model in the rat.

Greene¹,

1996

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The renin-angiotensin-aldosterone system (RAAS) participates in the injury sustained by the remnant kidney. Our studies assessed the importance of aldosterone in that model and the response of aldosterone to drugs interfering with the RAAS. Initially, four groups of rats were studied: SHAM-operated rats, untreated remnant rats (REM), REM rats treated with losartan and enalapril (REM AIIA), and REM AIIA rats infused with exogenous aldosterone (REM AIIA ϩ ALDO). The last group was maintained with aldosterone levels comparable to those in untreated REM rats by constant infusion of exogenous aldosterone. REM rats had larger adrenal glands and a Ͼ 10-fold elevation in plasma aldosterone compared to SHAM. REM AIIA rats demonstrated significant suppression of the hyperaldosteronism as well as marked attenuation of proteinuria, hypertension, and glomerulosclerosis compared to REM. REM AIIA ϩ ALDO rats manifested greater proteinuria, hypertension, and glomerulosclerosis than REM AIIA rats. Indeed, by 4 wk of observation all of these features of the experimental disease were similar in magnitude in REM AIIA ϩ ALDO and untreated REM. In separate REM rats spironolactone administration did not reduce glomerular sclerosis but did transiently reduce proteinuria, lowered arterial pressure, and lessened cardiac hypertrophy. In summary, aldosterone contributes to hypertension and renal injury in the remnant kidney model. (

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“…It is known that basal and stimulated K + efflux is elevated in arterial muscle from genetic and renal models of rat hypertension. 16 - 17 Therefore, it is possible that the response of arterial muscle K + channels to pressure is modified after chronic exposure to high blood pressure.…”

Section: -15mentioning

confidence: 99%

Pressure-induced activation of membrane K+ current in rat saphenous artery.

et al. 1992

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Pressurization of isolated arteries may result in Ca 2+-dependent contraction and membrane depolarization. Because the open state probability of some vascular muscle K + channels is augmented by rises in cytosolic Ca 2+ and membrane depolarization, we investigated the possibility that increases in intraluminal pressure activate K + channels in isolated, perfused rat saphenous arteries. Stepwise increases in intraluminal pressure from 5 to 205 mm Hg resulted in increasing, active arterial contraction, measured as smaller diameters in physiological salt solution than in Ca 2+ -free solution. Addition of 10 mM tetraethylammonium to the physiological salt solution to block arterial muscle K + channels caused progressively greater diameter reductions at pressures above 25 mm Hg. Microelectrode measurements of membrane potential showed that tetraethylammonium depolarized arterial muscle more at 105 mm Hg (16±1 mV) than at 25 mm Hg (10±l mV). The sensitivity of K + current to tetraethylammonium was also demonstrated in patch-clamped vascular muscle cells from the same arteries. Peak whole-cell K + current was suppressed 47% and 79% by 1 and 10 mM tetraethylammonium, respectively. This same current was enhanced 3.6-fold by the Ca 2+ ionophore A23187 (10 /iM), suggesting a Ca 2+ dependence. We conclude that increases in intraluminal pressure progressively activate tetraethylammonium-sensitive K + channels in the arterial muscle membrane. This can serve as a negative feedback mechanism to limit pressure-induced arterial constriction. (Hypertension 1992;19:725-729) KEY WORDS • vascular smooth muscle • tetraethylammonium compounds • blood pressure • calcium • potassium channels P ressure-induced contraction of arterial muscle minimizes arterial diameter changes during local blood pressure alterations. Many studies have focused on the mechanisms for Ca 2+ activation of arterial muscle in this response, as Ca 2+ influx appears to be required for myogenic activation.1 -4 However, the final level of arterial muscle contraction in response to changes in intraluminal pressure (IP) likely reflects the integrated reaction of multiple membrane ionic mechanisms. Of these, the function of arterial membrane K + channels has received scant attention, despite their recognized role as key modulators of arterial contraction and excitability. 5In view of this, the purpose of this study was to test the hypothesis that arterial membrane K + channels buffer the pressure-induced contraction of arterial muscle segments. Using tetraethylammonium (TEA) to block vascular muscle K + channels in perfused rat saphenous arteries, we estimated the contribution of K + current to arterial diameter and membrane potential (E m ) at IP values from 5 to 205 mm Hg. We used patch-clamp methods to document K + current sensitivity to TEA-induced block and to increases of cytosolic Ca 2+ in isolated arterial cells. The results suggest that activation of membrane K + channels may be a mechanism for attenuation of acute pressure-induced constriction in small arte...

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Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats.

Abstract: The purpose of this study was to evaluate the effect of calcium antagonists on basal tension and the elevated

Cited by 21 publications

References 31 publications

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Role of aldosterone in the remnant kidney model in the rat.

Pressure-induced activation of membrane K+ current in rat saphenous artery.

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Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats.

Abstract: The purpose of this study was to evaluate the effect of calcium antagonists on basal tension and the elevated

Cited by 21 publications

References 31 publications

Charybdotoxin‐sensitive K+ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Charybdotoxin‐sensitive K+ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Role of aldosterone in the remnant kidney model in the rat.

Pressure-induced activation of membrane K+ current in rat saphenous artery.

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Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats

Charybdotoxin‐sensitive K⁺ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats