ArticleThe Journal of clinical investigation1997
Cellular mechanisms mediating rat renal microvascular constriction by angiotensin II.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Tiny clue reveals the general trend: a bibliometric and visualized analysis of renal microcirculation.Renal failure · 2024Article
- Maladaptation of renal hemodynamics contributes to kidney dysfunction resulting from thoracic spinal cord injury in mice.American journal of physiology. Renal physiology · 2022Article
- Effects of SGLT2 inhibitors on eGFR in type 2 diabetic patients-the role of antidiabetic and antihypertensive medications.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Pharmacological inhibition of TRPV4 channels protects against ischemia-reperfusion-induced renal insufficiency in neonatal pigs.Clinical science (London, England : 1979) · 2019Article
- How the kidney hyperfiltrates in diabetes: From molecules to hemodynamics.World journal of diabetes · 2015Review
- Altered gap junctional communication and renal haemodynamics in Zucker fatty rat model of type 2 diabetes.Diabetologia · 2011Article
- Renal microvascular constriction to membrane depolarization and other stimuli: pivotal role for rho-kinase.Pflugers Archiv : European journal of physiology · 2006Article
- Relative contributions of Ca2+ mobilization and influx in renal arteriolar contractile responses to arginine vasopressin.American journal of physiology. Renal physiology · 2005Article
- Tyrosine kinase involvement in renal arteriolar constrictor responses to angiotensin II.Hypertension (Dallas, Tex. : 1979) · 2001Article
- Mechanosensitive cation channels mediate afferent arteriolar myogenic constriction in the isolated rat kidney.The Journal of physiology · 1998Article
- Altered electromechanical coupling in the renal microvasculature during the early stage of diabetes mellitus.Clinical and experimental pharmacology & physiologyReview
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Authors and funding
8 authors.
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Abstract
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+/-3 (n = 8, P < 0.01) and 27+/-3% (n = 8, P < 0.01), respectively. Subsequent addition of nifedipine restored AA but not EA diameter. Manganese (8 mM) reversed EA constriction by 65+/-9% (P < 0.01). In the second group, the addition of N-ethylmaleimide (10 microM), a Gi/Go protein antagonist, abolished AngII- induced EA (n = 6) but not AA constriction (n = 6). In the third series of experiments, treatment with 2-nitro-4-carboxyphenyl-N, N-diphenyl-carbamate (200 microM), a phospholipase C inhibitor, blocked both AA and EA constriction by AngII (n = 6 for each). In the fourth group, thapsigargin (1 microM) prevented AngII-induced AA constriction (n = 8) and attenuated EA constriction (8+/-2% decrease in EA diameter at 0.3 nM AngII, n = 8, P < 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.
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