Effects of insulin on rat renal microvessels

Studies in the isolated perfused hydronephrotic kidney

K. Hayashi, K. Fujiwara, K. Oka, T. Nagahama, H. Matsuda, T. Saruta

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Although insulin is demonstrated to decrease vascular tone, the role of insulin in renal microcirculation has not been fully determined. In the present study, the effect of insulin on renal microvascular tone was assessed using the isolated perfused hydronephrotic rat kidney. Insulin (300 μU/ml) had no effect on the basal renal microvessel diameter. In addition, insulin did not alter myogenic (that is, pressure-induced) constriction of preglomerular microvessels, with similar magnitude of constriction observed in response to elevated renal perfusion pressure from 80 to 180 mm Hg (interlobular artery, -23 ± 3% vs, -19 ± 4%; afferent arteriole, -22 ± 3% vs. -21 ± 4%, for control and insulin, respectively). In striking contrast, insulin dose-dependently reversed the norepinephrine (NE)-induced tone of interlobular arteries, afferent arterioles, and efferent arterioles, with 94 ± 9%, 104 ± 6%, and 86 ± 10% reversal at 300 μU/ml, respectively. These vasodilator actions were markedly inhibited by N-Arg; in the presence of N- Arg, insulin (300 μU/ml) exerted only a modest dilator action on interlobular arteries (24 ± 9% reversal), afferent arterioles (23 ± 10% reversal), and efferent arterioles (14 ± 9% reversal). A similar renal microvascular responsiveness to insulin was also observed during angiotensin II (Ang II)-induced constriction. In conclusion, the ability of insulin to dilate the renal microvasculature differs, with marked inhibitory action during NE/Ang II-induced constriction and almost no inhibition during myogenic constriction. Furthermore, the present study suggests that the insulin-induced renal vasodilation is mediated by nitric oxide.

Original languageEnglish
Pages (from-to)1507-1513
Number of pages7
JournalKidney International
Volume51
Issue number5
Publication statusPublished - 1997

Fingerprint

Microvessels
Insulin
Kidney
Arterioles
Constriction
Arteries
Angiotensin II
Norepinephrine
Pressure
Microcirculation
Vasodilator Agents
Vasodilation
Blood Vessels
Nitric Oxide
Perfusion

ASJC Scopus subject areas

  • Nephrology

Cite this

Hayashi, K., Fujiwara, K., Oka, K., Nagahama, T., Matsuda, H., & Saruta, T. (1997). Effects of insulin on rat renal microvessels: Studies in the isolated perfused hydronephrotic kidney. Kidney International, 51(5), 1507-1513.

Effects of insulin on rat renal microvessels : Studies in the isolated perfused hydronephrotic kidney. / Hayashi, K.; Fujiwara, K.; Oka, K.; Nagahama, T.; Matsuda, H.; Saruta, T.

In: Kidney International, Vol. 51, No. 5, 1997, p. 1507-1513.

Research output: Contribution to journalArticle

Hayashi, K, Fujiwara, K, Oka, K, Nagahama, T, Matsuda, H & Saruta, T 1997, 'Effects of insulin on rat renal microvessels: Studies in the isolated perfused hydronephrotic kidney', Kidney International, vol. 51, no. 5, pp. 1507-1513.
Hayashi K, Fujiwara K, Oka K, Nagahama T, Matsuda H, Saruta T. Effects of insulin on rat renal microvessels: Studies in the isolated perfused hydronephrotic kidney. Kidney International. 1997;51(5):1507-1513.
Hayashi, K. ; Fujiwara, K. ; Oka, K. ; Nagahama, T. ; Matsuda, H. ; Saruta, T. / Effects of insulin on rat renal microvessels : Studies in the isolated perfused hydronephrotic kidney. In: Kidney International. 1997 ; Vol. 51, No. 5. pp. 1507-1513.
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AB - Although insulin is demonstrated to decrease vascular tone, the role of insulin in renal microcirculation has not been fully determined. In the present study, the effect of insulin on renal microvascular tone was assessed using the isolated perfused hydronephrotic rat kidney. Insulin (300 μU/ml) had no effect on the basal renal microvessel diameter. In addition, insulin did not alter myogenic (that is, pressure-induced) constriction of preglomerular microvessels, with similar magnitude of constriction observed in response to elevated renal perfusion pressure from 80 to 180 mm Hg (interlobular artery, -23 ± 3% vs, -19 ± 4%; afferent arteriole, -22 ± 3% vs. -21 ± 4%, for control and insulin, respectively). In striking contrast, insulin dose-dependently reversed the norepinephrine (NE)-induced tone of interlobular arteries, afferent arterioles, and efferent arterioles, with 94 ± 9%, 104 ± 6%, and 86 ± 10% reversal at 300 μU/ml, respectively. These vasodilator actions were markedly inhibited by N-Arg; in the presence of N- Arg, insulin (300 μU/ml) exerted only a modest dilator action on interlobular arteries (24 ± 9% reversal), afferent arterioles (23 ± 10% reversal), and efferent arterioles (14 ± 9% reversal). A similar renal microvascular responsiveness to insulin was also observed during angiotensin II (Ang II)-induced constriction. In conclusion, the ability of insulin to dilate the renal microvasculature differs, with marked inhibitory action during NE/Ang II-induced constriction and almost no inhibition during myogenic constriction. Furthermore, the present study suggests that the insulin-induced renal vasodilation is mediated by nitric oxide.

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