Angiotensin actions in the kidney: Renewed insight into the old hormone

Ichikawa, Iekuni; Harris, Raymond C.

doi:10.1038/ki.1991.249

Cited by 270 publications

(110 citation statements)

References 117 publications

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“…These facts support the proposal that the beneficial effects of ACE-I on the progression of nephropathy may be independent of its antihypertensive properties [21,25]. The mechanism may be due to the beneficial effect of ACE-I on the glomerular extracellular matrix by 1) improving glomerular haemodynamics [26][27][28] and/or 2) inhibiting trophic properties of angiotensin II to promote glomerular hypertrophy and accumulation of mesangial matrix [26,29,30].…”

Section: Discussionsupporting

confidence: 71%

Predictors of the progression of diabetic nephropathy and the beneficial effect of angiotensin-converting enzyme inhibitors in NIDDM patients

et al. 1997

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Section: Discussionsupporting

confidence: 71%

Predictors of the progression of diabetic nephropathy and the beneficial effect of angiotensin-converting enzyme inhibitors in NIDDM patients

et al. 1997

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“…In addition to its physiological actions on glomerular hemodynamics and excretory function (1), AngII has been shown to play an important role in mediating pathophysiological renal vasoconstriction in a wide array of disorders, including heart failure, hypertension, and progressive renal diseases (2). Thus, previous studies have demonstrated that angiotensin-converting enzyme inhibition induces beneficial effects on renal functions under the conditions mentioned above (3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

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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“…There is evidence that in the proximal tubule Ang II is coupled to a pertussis toxin-sensitive G i , reducing adenylate cyclase activity and cAMP accumulation. This appears to be the mechanism by which Ang II stimulates proximal tubule bicarbonate absorption (26). In addition, G protein-coupled activation of phospholipase A 2 with subsequent metabolization of arachidonic acid by cytochrome P450 epoxygenase to epoxy-eicosa-trienoic acids (EET) apparently mediates the natriuretic effect of Ang II acting on luminal angiotensin receptors (42).…”

Section: Renal Actions Of Angiotensin IImentioning

confidence: 99%

“…In the physiological concentration range, Ang II acts mainly as an antinatriuretic hormone by directly or indirectly producing changes in renal hemodynamics and in sodium reabsorption (25). Considerable evidence suggests that the intrarenal actions of Ang II are quantitatively more important than the extrarenal mechanisms in the normal day-today regulation of sodium and water excretion (23,26).…”

Section: Renal Actions Of Angiotensin IImentioning

confidence: 99%

“…The efferent arteriolar vasoconstriction would reduce the peritubular capillary hydrostatic pressure as well as increase peritubular capillary colloid osmotic pressure due to an increase in the filtration fraction. Both of these changes would tend to decrease renal interstitial fluid hydrostatic pressure and raise interstitial fluid colloid osmotic pressure, thereby increasing the driving force for fluid reabsorption (26,34).…”

Section: Renal Actions Of Angiotensin IImentioning

confidence: 99%

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Renal actions of angiotensin-(1-7)

Silva¹,

Baracho²,

Passaglio³

et al. 1997

Braz J Med Biol Res

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The heptapeptide angiotensin-(1-7) is considered to be a biologically active endproduct of the renin-angiotensin system. This angiotensin, which is devoid of the most known actions of angiotensin II such as induction of drinking behavior and vasoconstriction, has several selective effects in the brain and periphery. In the present article we briefly review recent evidence for a physiological role of angiotensin-(1-7) in the control of hydroelectrolyte balance.

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Angiotensin actions in the kidney: Renewed insight into the old hormone

Cited by 270 publications

References 117 publications

Predictors of the progression of diabetic nephropathy and the beneficial effect of angiotensin-converting enzyme inhibitors in NIDDM patients

Predictors of the progression of diabetic nephropathy and the beneficial effect of angiotensin-converting enzyme inhibitors in NIDDM patients

Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.

Renal actions of angiotensin-(1-7)

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