Vasomotion and Vasoconstriction Induced by a Ca++-Agonist in the Split Hydronephrotic Kidney

Steinhausen, M; Baehr, M.; Dussel, R.

doi:10.1159/000416449

Cited by 18 publications

(11 citation statements)

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“…Previous data using various methods imply that voltagedependent calcium channels are lacking in the efferent arteriole (14,41,42). Consistent with this, our recent results indicated that isradipine (0.1 M), a calcium antagonist, reversed AngII-induced afferent but not efferent arteriolar constriction (8).…”

Section: Discussionsupporting

confidence: 88%

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Takenaka¹,

Suzuki²,

Fujiwara³

et al. 1997

J. Clin. Invest.

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To assess cellular mechanisms mediating afferent (AA) and efferent arteriolar (EA) constriction by angiotensin II (AngII), experiments were performed using isolated perfused hydronephrotic kidneys. In the first series of studies, AngII (0.3 nM) constricted AAs and EAs by 29 Ϯ 3 ( n ϭ 8, P Ͻ 0.01) and 27 Ϯ 3% ( n ϭ 8, P Ͻ 0.01), respectively. Subsequent addition of nifedipine restored AA but not EA diameter. Manganese (8 mM) reversed EA constriction by 65 Ϯ 9% ( P Ͻ 0.01). In the second group, the addition of N -ethylmaleimide (10 M), a Gi/Go protein antagonist, abolished AngIIinduced EA ( n ϭ 6) but not AA constriction ( n ϭ 6). In the third series of experiments, treatment with 2-nitro-4-carboxyphenyl-N , N -diphenyl-carbamate (200 M), a phospholipase C inhibitor, blocked both AA and EA constriction by AngII ( n ϭ 6 for each). In the fourth group, thapsigargin (1 M) prevented AngII-induced AA constriction ( n ϭ 8) and attenuated EA constriction (8 Ϯ 2% decrease in EA diameter at 0.3 nM AngII, n ϭ 8, P Ͻ 0.05). Subsequent addition of manganese (8 mM) reversed EA constriction. Our data provide evidence that in AAs, AngII stimulates phospholipase C with subsequent calcium mobilization that is required to activate voltage-dependent calcium channels. Our results suggest that AngII constricts EAs by activating phospholipase C via the Gi protein family, thereby eliciting both calcium mobilization and calcium entry. ( J.

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Section: Discussionsupporting

confidence: 88%

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Takenaka¹,

Suzuki²,

Fujiwara³

et al. 1997

J. Clin. Invest.

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“…Bay K 8644 acts directly and specifically on L-type VGCCs to prolong their open state (16)(17)(18). Studies using the in vivo hydronephrotic kidney first unveiled the ability of this compound to evoke preglomerular vasoconstriction without significantly altering efferent arteriolar diameter (23). The preferential impact of Bay K 8644 on the preglomerular microvasculature of the normal rat kidney is confirmed by our observations.…”

Section: Discussionsupporting

confidence: 73%

Functional impairment of renal afferent arteriolar voltage-gated calcium channels in rats with diabetes mellitus.

Carmines¹,

Ohishi²,

Ikenaga³

1996

J. Clin. Invest.

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Experiments were performed to test the hypothesis that diabetes mellitus is associated with impaired afferent arteriolar responsiveness to opening of voltage-gated calcium channels. Diabetes was induced by injection of streptozocin (65 mg/kg, i.v.) and insulin was administered via an osmotic minipump to achieve moderate hyperglycemia. Sham rats received vehicle treatments. 2 wk later, the in vitro bloodperfused juxtamedullary nephron technique was used to al-

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“…17 In the efferent arteriole, however, L-type calcium channels appear sparse because efferent arterioles are refractory to the vasodilator action of the calcium antagonist 4 -6 or the vasoconstrictor action of BAY K-8644, an L-type calcium agonist. 27 Furthermore, the present study shows that during the blockade of L-type calcium channels by nifedipine, mibefradil retains the ability to dilate the efferent arteriole. Collectively, these observations provide strong evidence for the mechanism of mibefradil-induced efferent arteriolar dilation that is independent of L-type calcium channel blockade but rather is associated with the inhibition of T-type calcium channelmediated mechanisms.…”

Section: Ozawa Et Al T-type Calcium Channels In Renal Microcirculationsupporting

confidence: 56%

Effect of T-Type Selective Calcium Antagonist on Renal Microcirculation

et al. 2001

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Abstract-Although calcium antagonists exert preferential vasodilation of renal afferent arterioles, we have recently demonstrated that nilvadipine and efonidipine, possessing both L-type and T-type calcium channel blocking action, reverse the angiotensin (Ang) II-induced afferent and efferent arteriolar constriction. In the present study, we investigated the role of T-type calcium channels in mediating the Ang II-induced efferent arteriolar tone using the selective T-type calcium channel blocker mibefradil. Isolated perfused hydronephrotic rat kidneys were used for direct visualization of renal microcirculation. Administration of Ang II (0.3 nmol/L) caused marked constriction of afferent (from 13.5Ϯ0.6 to 9.2Ϯ0.6 m, PϽ0.01, nϭ6) and efferent (from 11.5Ϯ1.0 to 7.4Ϯ0.7 m, PϽ0.01, nϭ5) arterioles. Mibefradil (1 mol/L) dilated both vessels, with 82Ϯ11% and 72Ϯ7% reversal of afferent and efferent arterioles, respectively. Similarly, nickel chloride (100 mol/L) caused dilation of both arterioles, similar in magnitude in afferent (68Ϯ10%, nϭ7) and efferent (80Ϯ7%, nϭ7) arterioles. To eliminate the possibility that the mibefradil-induced dilation was mediated by L-type channel blockade, mibefradil was administered in the presence of nifedipine (1 mol/L). Thus, nifedipine caused modest efferent arteriolar dilation (30Ϯ6% reversal, nϭ9), and subsequent addition of mibefradil elicited further dilation of this vessel (80Ϯ4%, PϽ0.01 versus nifedipine). Furthermore, mibefradil reversed the Ang II-induced efferent arteriolar constriction even in the presence of nifedipine and phentolamine. These findings demonstrate that T-type calcium antagonists markedly dilate the Ang II-induced efferent arteriolar constriction, but the action is not mediated by inhibition of catecholamine release. This potent activity would contribute to the efferent arteriolar response to nilvadipine and efonidipine and may offer benefit in light of glomerular hemodynamics. Key Words: mibefradil Ⅲ afferent arteriole Ⅲ efferent arteriole Ⅲ T-type calcium channel Ⅲ calcium antagonists Ⅲ renal microcirculation A growing body of evidence has accrued that the calcium antagonist, a blocker of L-type voltage-dependent calcium channels, exerts potent renal vasodilatory action in the face of systemic hypotension. 1 This unique action is frequently accompanied by an elevation in glomerular filtration rate and filtration fraction. 2,3 To elucidate the mechanism for calcium antagonist-induced alterations in renal hemodynamics, several lines of recent investigations indicate that the calcium antagonist elicits predominant dilation of the afferent arteriole but modest action on the efferent arteriole. 4 -6 These observations are endorsed by the fact that L-type voltagedependent calcium channels prevail functionally in the afferent arteriole but are silent in the efferent arteriole. 7,8 Such a preferential role of voltage-dependent calcium channels in the afferent arteriole thus favors the elevation in glomerular filtration rate by the calcium antagonist. 2,3 In contra...

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Vasomotion and Vasoconstriction Induced by a Ca++-Agonist in the Split Hydronephrotic Kidney

Cited by 18 publications

References 0 publications

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Functional impairment of renal afferent arteriolar voltage-gated calcium channels in rats with diabetes mellitus.

Effect of T-Type Selective Calcium Antagonist on Renal Microcirculation

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