Effects of insulin-like growth factor I on the renal juxtamedullary microvasculature

Burkhard Tönshoff, Frederick J. Kaskel, Leon C. Moore

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

To characterize the effects on the rat renal preglomerular microvasculature of insulin-like growth factor I (IGF-I), experiments were performed using the in vitro blood-perfused juxtamedullary nephron preparation. IGF-I induced a reversible vasodilation of pre-but not postglomerular microvessels in a dose-dependent manner (10-9-10-7 M). The IGF-I-induced vasodilation was similar in all preglomerular vascular segments: interlobular artery, 11.5 ± 1.2% of control (n = 16); mid-afferent arterioles, 11.6 ± 1.7% (n = 24); and juxtaglomerular afferent segments, 16.1 ± 2.8% (n = 19). Renal autoregulatory capacity was not reduced by IGF- I. Pretreatment with the nitric oxide (NO) synthase inhibitor N(G)-nitro-L- arginine methyl ester (10-4 M) completely inhibited the vasodilatory response to IGF-I. IGF-I induced a rapid increase of NO concentration in intact renal microvessels, monitored by a NO-selective voltametric microelectrode. Pretreatment with the cyclooxygenase inhibitor indomethacin (10-5 M) not only abrogated the IGF-I-induced dilation, but, moreover, IGF- I elicited a small but significant (~10%) vasoconstriction in all preglomerular vessels. These results indicate that the renal vascular effects of IGF-I involve activation of two endogenous vasodilators (NO and vasodilatory prostaglandins). In addition, IGF-I may also release an undefined vasoconstrictor.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Physiology
Volume274
Issue number1 43-1
StatePublished - Jan 1998
Externally publishedYes

Fingerprint

Microvessels
Insulin-Like Growth Factor I
Kidney
Nitric Oxide
Vasodilation
Blood Vessels
Cyclooxygenase Inhibitors
NG-Nitroarginine Methyl Ester
Nephrons
Arterioles
Microelectrodes
Vasoconstrictor Agents
Vasoconstriction
Nitric Oxide Synthase
Indomethacin
Prostaglandins
Dilatation
Arteries

Keywords

  • Nitric oxide
  • Nitric oxide electrode
  • Prostaglandins
  • Renal autoregulation
  • Renal microcirculation

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Effects of insulin-like growth factor I on the renal juxtamedullary microvasculature. / Tönshoff, Burkhard; Kaskel, Frederick J.; Moore, Leon C.

In: American Journal of Physiology - Renal Physiology, Vol. 274, No. 1 43-1, 01.1998.

Research output: Contribution to journalArticle

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abstract = "To characterize the effects on the rat renal preglomerular microvasculature of insulin-like growth factor I (IGF-I), experiments were performed using the in vitro blood-perfused juxtamedullary nephron preparation. IGF-I induced a reversible vasodilation of pre-but not postglomerular microvessels in a dose-dependent manner (10-9-10-7 M). The IGF-I-induced vasodilation was similar in all preglomerular vascular segments: interlobular artery, 11.5 ± 1.2{\%} of control (n = 16); mid-afferent arterioles, 11.6 ± 1.7{\%} (n = 24); and juxtaglomerular afferent segments, 16.1 ± 2.8{\%} (n = 19). Renal autoregulatory capacity was not reduced by IGF- I. Pretreatment with the nitric oxide (NO) synthase inhibitor N(G)-nitro-L- arginine methyl ester (10-4 M) completely inhibited the vasodilatory response to IGF-I. IGF-I induced a rapid increase of NO concentration in intact renal microvessels, monitored by a NO-selective voltametric microelectrode. Pretreatment with the cyclooxygenase inhibitor indomethacin (10-5 M) not only abrogated the IGF-I-induced dilation, but, moreover, IGF- I elicited a small but significant (~10{\%}) vasoconstriction in all preglomerular vessels. These results indicate that the renal vascular effects of IGF-I involve activation of two endogenous vasodilators (NO and vasodilatory prostaglandins). In addition, IGF-I may also release an undefined vasoconstrictor.",
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