Intrarenal vascular effects of angiotensin I and angiotensin II

Britton, Steven L.

doi:10.1152/ajpheart.1981.240.6.h914

Cited by 8 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is consistent with the considerable evidence that shows that the renovascular bed is more sensitive than the systemic vasculature to Ang II. [12][13][14][15][16] On the other hand, blocking the ET receptors (group 2, period 1) caused the same small decline in MAP as Ang II blockade but had an insignificant effect on RBF. A fall in RBF only became apparent after NO was blocked.…”

Section: Relative Role Of Ang II Through Its At 1 Receptor Et No Amentioning

confidence: 99%

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

Gómez-Alamillo¹,

Juncos²,

Cases³

et al. 2003

Hypertension

View full text Add to dashboard Cite

Abstract-We examined whether interactions between angiotensin II (Ang II), endothelin (ET), nitric oxide (NO), and prostaglandins (PGs) differentially regulate perfusion to distinct vascular beds. For this, we blocked either angiotensin AT 1 or ET receptors or both and then sequentially inhibited NO and PG synthesis in anesthetized dogs. Blocking Ang II or ET had similar effects on systemic hemodynamics: Mean arterial pressure fell slightly without altering cardiac output. Blocking both caused a synergistic fall in mean arterial pressure and increased cardiac output. Pulmonary vascular resistance was not altered by blocking Ang II, ET, or both but progressively increased during NO and PG blockade in group 2 (which had unblocked ET receptors), suggesting that endogenous ET exerts pulmonary vasoconstriction that is tempered by NO and PGs. In the kidney, blocking Ang II increased regional blood flow (RBF), glomerular filtration rate (GFR), and fractional excretion of sodium (FENa). In contrast, blocking ET did not alter RBF, and it decreased GFR and FENa. Combined Ang II and ET blockade markedly increased RBF without altering GFR, and FENa was maintained at the levels as when only ET was blocked. Sequentially inhibiting NO and PGs decreased RBF when Ang II or ET were blocked but had little effect when both were blocked. Finally, Ang II or ET blockade did not alter iliac blood flow. Inhibiting NO and PGs decreased iliac blood flow when Ang II or ET but not both were blocked. These results suggest that regional differences in the interactions between endogenous Ang II, ET, NO, and PGs are important determinants in systemic, pulmonary, and regional hemodynamics. Key Words: endothelin Ⅲ angiotensin II Ⅲ nitric oxide Ⅲ prostaglandins Ⅲ hemodynamics Ⅲ natriuresis T he maintenance of mean arterial pressure (MAP) depends on a critical equilibrium between renal perfusion and systemic blood pressure. 1 In general, increments of renal perfusion pressure trigger compensatory mechanisms that tend to lower MAP, whereas the opposite occurs when renal perfusion pressure is decreased. To a large extent, these cardiorenal interactions are enacted by the participation of humoral systems such as renin angiotensin, prostaglandins (PGs), nitric oxide (NO) and as revealed in more recent studies by endothelin (ET). Because of this, numerous studies have evaluated the effects of angiotensin II (Ang II), ET, NO donors, and PGs by infusing 2-5 or blocking one or more of these vasoactive factors. 6 -10 However, the relative role that each one of these vasoactive factors plays in regulating regional hemodynamics remains incompletely understood. Therefore, the aim of the present study was to determine the relative role of endogenous Ang II, ET, NO, and PGs (as well as their interactions) in regulating systemic and regional hemodynamics (with particular emphasis on renal function) in normal anesthetized dogs. For this purpose, we blocked the effects of either Ang II with the intravenous administration of L158,810 (a selective AT 1 receptor antag...

show abstract

Section: Relative Role Of Ang II Through Its At 1 Receptor Et No Amentioning

confidence: 99%

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

Gómez-Alamillo¹,

Juncos²,

Cases³

et al. 2003

Hypertension

View full text Add to dashboard Cite

show abstract

“…In mammalian kidneys ANG II may act on arterioles to redistribute blood flow, may contribute to the tubuloglomerular feedback mechanism responsible for autoregulation of the glomerular filtration rate, and also may affect tubular transport of ions (208)(209)(210)(211). However, even in modern mammals such as the rat, many granular cells of the vascular component are so distant from the distal tubule as to be removed from direct interactions (21).…”

Section: Winter 1984mentioning

confidence: 99%

The Renin-Angiotensin System in Nonmammalian Vertebrates*

Wilson

1984

Endocrine Reviews

View full text Add to dashboard Cite

The most primitive components of the RAS appeared early in the phylogenetic history of vertebrate animals. It is probable that renin granules were present in the kidneys of ancestral chordates before divergence in the evolution of actinopterygian fish and tetrapods occurred. Granulated juxtaglomerular cells similar to the renin-containing cells of the mammalian nephron are found in most extant vertebrate species although not in agnathan and elasmobranch fish. A macula densa occurs in amphibians, birds and mammals; and an extraglomerular mesangium, only in birds and mammals. Renin-like activity and angiotensin-like pressor material have been demonstrated in all classes of vertebrates. The amino acid sequences of native ANG I have been determined for representative species of teleost fish, amphibian, reptile and bird. These peptides differ from mammalian angiotensins at positions 1, 5 and 9. The RAS appears to be involved in osmoregulation, ionoregulation and the control of blood circulation. Prolonged hypovolemic hypotension or sodium depletion increases renin levels. Angiotensins elicit drinking and stimulate transepithelial ion transport. However, direct steroidogenic and antidiuretic hormone-releasing activities, which would promote mineral and fluid conservation, have not been demonstrated unambiguously in nonmammalian vertebrates. ANG II raises blood pressure by direct vasoconstrictor action on arteriolar muscles in some animals, but perhaps more generally by acting on the nervous system and adrenal paraneurons. In birds the hormone also has a hypotensive effect. ANG II stimulates the SNS in agnathans, elasmobranchs, teleosts, amphibians, reptiles, birds and mammals. Thus, modulation of sympathetic activity may be one of the most primitive and conservative functions of the RAS. For this reason, nonmammalian vertebrates are valuable models for studying the neurogenic actions of angiotensin II relevant to hypertensive disease.

show abstract

The localization of converting enzyme in kidney vessels of the rat

Taugner

Ganten

1982

Histochemistry

View full text Add to dashboard Cite

An antibody against pure rabbit lung converting enzyme (CE) showing cross-reaction with CE from other species was used for immunocytochemical studies in the kidney of rats. Using the indirect labelling PAP-technique, specific immunostaining was found in the endothelial layer of all arteries and arterioles of kidney cortex and in some descending vasa recta. CE-positive reactions were also seen in most glomeruli, the reaction product being confined to only a few capillary loops in connection with the glomerular stalk. A few immunostained capillaries in the cortical labyrinth were suspected to belong to the first ramifications of the efferent arteriole. The bulk of all other of the glomerular and peritubula capillaries as well as all veins of the kidney showed no obvious immunostaining. The functional significance of this specific localization pattern of CE in the endothelium of kidney vessels is discussed with respect to the actions of the systemic and the local, intrarenal renin-angiotensin-system on kidney functions.

show abstract

Intrarenal vascular effects of angiotensin I and angiotensin II

Cited by 8 publications

References 0 publications

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

Interactions Between Vasoconstrictors and Vasodilators in Regulating Hemodynamics of Distinct Vascular Beds

The Renin-Angiotensin System in Nonmammalian Vertebrates*

The localization of converting enzyme in kidney vessels of the rat

Contact Info

Product

Resources

About