Evidence for a noradrenergic innervation to α<sub>1A</sub>‐adrenoceptors in rat kidney

Blue, David R.; Vimont, Rachel L.; Clarke, David E.

doi:10.1111/j.1476-5381.1992.tb12760.x

Cited by 34 publications

(26 citation statements)

References 12 publications

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“…This would indicate that the postsynaptic a 1A -and a 1D -adrenoceptor subtypes are involved in mediating the constrictions. The predominant involvement of a 1A -adrenoceptor in mediating renal vasoconstrictor responses has been reported previously in other models of hypertension (Sattar & Johns, 1991;1994a, b;Blue et al, 1992;. Furthermore, there has been the suggestion of an involvement of a 1D -as well as a 1A -adrenoceptors in mediating renal vasoconstriction (VillalobosMolina & Ibarra, 1996;1997).…”

Section: A Armenia Et Al Renal Adrenoceptors In Diabetes and Hypertesupporting

confidence: 65%

“…Within the kidney, a 1A -adrenoceptors have been consistently found to predominate over the a 1B and a 1D , both in terms of density and functionality (Clarke et al, 1990;Han et al, 1990;Eltze et al, 1991;Blue et al, 1992;Elhawary et al, 1992;Stassen et al, 1998). Activation of a 1A -adrenoceptors causes constriction of the renal vascular resistance bed (afferent and efferent arterioles) in the Wistar, Stroke-Prone Spontaneously Hypertensive Rats (SHRSP), Two kidney One Clip (2K1C) and Deoxycorticosterone acetate-Salt (DOCA-Salt) hypertensive rats, while the a 1B adrenoceptor subtype seems to play a lesser role (Sattar & Johns, 1994a, b).…”

Section: Introductionmentioning

confidence: 99%

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The contribution of adrenoceptor subtype(s) in the renal vasculature of diabetic spontaneously hypertensive rats

Armenia

Munavvar

Abdullah

et al. 2004

British J Pharmacology

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1 Diabetes and hypertension are both associated with an increased risk of renal disease and are associated with neuropathies, which can cause defective autonomic control of major organs including the kidney. This study aimed to examine the a 1 -adrenoceptor subtype(s) involved in mediating adrenergically induced renal vasoconstriction in a rat model of diabetes and hypertension. 2 Male spontaneously hypertensive rats (SHR), 220-280 g, were anaesthetized with sodium pentobarbitone 7-day poststreptozotocin (55 mg kg À1 i.p.) treatment. The reductions in renal blood flow (RBF) induced by increasing frequencies of electrical renal nerve stimulation (RNS), close intrarenal bolus doses of noradrenaline (NA), phenylephrine (PE) or methoxamine were determined before and after administration of nitrendipine (Nit), 5-methylurapidil (5-MeU), chloroethylclonidine (CEC) and BMY 7378. 3 In the nondiabetic SHR group, mean arterial pressure (MAP) was 14676 mmHg, RBF was 28.071.4 ml min À1 kg À1 and blood glucose was 112.374.7 mg dl À1, and in the diabetic SHR Group, MAP was 14473 mmHg, RBF 26.971.3 ml À1 min kg À1 and blood glucose 316.2710.5 mg dl À1. Nit, 5-MeU and BMY 7378 blunted all the adrenergically induced renal vasoconstrictor responses in SHR and diabetic SHR by 25-35% (all Po0.05), but in diabetic rats the responses induced by RNS and NA treated with 5-MeU were not changed. By contrast, during the administration of CEC, vasoconstrictor responses to all agonists were enhanced by 20-25% (all Po0.05) in both the SHR and diabetic SHR. 4 These findings suggest that a 1A and a 1D -adrenoceptor subtypes contribute in mediating the adrenergically induced constriction of the renal vasculature in both the SHR and diabetic SHR. There was also an indication of a greater contribution of presynaptic adrenoceptors, that is, a 1B -, and/or a 2 -subtypes.

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Section: A Armenia Et Al Renal Adrenoceptors In Diabetes and Hypertesupporting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

The contribution of adrenoceptor subtype(s) in the renal vasculature of diabetic spontaneously hypertensive rats

Armenia

Munavvar

Abdullah

et al. 2004

British J Pharmacology

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“…Since CEC selectively inhibited sympathetic adrenergic vasoconstriction, but did not aect the purinergic response in this study, it is unlikely that CEC acts by stimulating prejunctional adrenoceptors. In addition, in the rat perfused kidney, CEC at a high concentration (100 mM) is unable to aect the nerve stimulation-induced release of NA (Blue et al, 1992). Thus, an alternative possibility is that neuronal and exogenous NA-induced responses might be mediated by dierent subtypes of a 1 -adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

“…Recent observations further con®rmed these dierences in the same preparation and indicated that the a 1 -adrenoceptor subtype involved in the nerve-stimulated response resembled the a 1D -adrenoceptor subtype (Honner & Docherty, 1999). However, in rat blood vessel preparations, nerve-stimulated NA and exogenously applied NA may couple to the same subtype of a 1 -adrenoceptors, i.e., a 1A -adrenoceptors for the rat mesenteric arterial bed (Kong et al, 1994;Williams & Clarke, 1995) and the vasculature of rat kidney (Blue et al, 1992), a 1B -adrenoceptors for the rat irideal blood vessel (Gould & Hill, 1994). An a 1 -adrenoceptor has been identi®ed as a functional subtype for vasoconstriction of the canine splenic artery to both neuronal and exogenous NA (Ren et al, 1994a,b;1996).…”

Section: Introductionmentioning

confidence: 99%

Existence of different α₁‐adrenoceptor subtypes in junctional and extrajunctional neurovascular regions in canine splenic arteries

Yang

Chiba

2001

British J Pharmacology

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1 The present study attempted to characterize the a 1 -adrenoceptor subtypes mediating vasoconstrictor responses to administered and nerve stimulation-evoked noradrenaline (NA) release in the isolated and perfused canine splenic artery. 2 A previous study demonstrated that periarterial electrical nerve stimulation (30 s trains of pulses at a frequency of 1, 4 or 10 Hz) induced a double peaked vasoconstriction consisting of an initial transient, predominantly P2X-purinoceptor-mediated constriction followed by a prolonged, mainly a 1 -adrenoceptor-mediated response in the canine splenic artery. 3 The eects of a 1 -adrenoceptor subtype antagonists on neuronally-mediated second peaked vasoconstrictions were analysed. BMY 7378 (10 ± 100 nM), a selective a 1D -adrenoceptor antagonist produced a dose-dependent inhibition of the second peak responses at all frequencies used. BMY 7378 (100 nM) reduced these responses by approximately 30%. Exposure of tissues to chloroethylclonidine (CEC, 60 mM), a selective a 1B -adrenoceptor antagonist attenuated the second peak response by approximately 60%, even in the presence of BMY 7378 (100 nM). On the other hand, WB 4101 (100 nM), a selective a 1A -adrenoceptor antagonist potentiated nerve-stimulationevoked double peaked vasoconstrictions, especially at low frequencies (1 and 4 Hz). 4 Vasoconstrictor responses to administered NA were dose-dependently antagonized by WB 4101 (10 ± 100 nM), but were not signi®cantly aected by either BMY 7378 (10 ± 100 nM) or by CEC (60 mM). 5 The present results indicate that NA released from sympathetic nerves may junctionally exert its vasoconstrictor eect via activation of postjunctional a 1B -and in part a 1D -adrenoceptors, whereas exogenous NA extrajunctionally activates a 1A -adrenoceptors to produce its vascular action in canine splenic arteries.

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“…Furthermore we have demonstrated that this reduction in constrictor function can be attributed, at least in part, to the a 1A -adrenergic receptor. When coupled with the reported evidence that a-adrenergic receptors are the primary receptors that mediate changes in renal vascular resistance during sympathetic activation (Wolff et al 1987;Blue et al 1992), a loss of this type constrictor function could translate into lower preglomerular resistance resulting in higher glomerular pressures. Secondly, four to six months male and female Munich Wistar rats both reached maximum constriction at 1 Â 10 j3 M phenylephrine, and there was no gender difference at that time ( Figure 4A).…”

Section: Discussionmentioning

confidence: 96%

Decreased alpha-adrenergic constriction of renal preglomerular arteries occurs with age and is gender-specific in the rat

Falcone

Joshua

Passmore

2005

AGE

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Age and/or gender appear to moderate alpha-adrenergic mediated constrictor mechanisms found in the interlobar arteries of the Munich Wistar rat. We have determined the extent of constriction to alpha-adrenergic receptor stimulation using norepinephrine, phenylephrine and A61603 (a 1A -adrenergic receptor agonist) as a function of age and gender. Norepinephrine produced less constriction in male-derived arteries at ages greater than eight months as compared to the younger adult male (four to six months). The arteries derived from females did not demonstrate altered constriction until greater than 15 months of age. Similarly, arteries derived from the male demonstrated weaker constrictions to phenylephrine (10 j6 to 10 j3 M) at ages greater than eight months while arteries from females showed differences at greater than 15 months. In contrast, the effective concentration of norepinephrine to cause a 50% maximal constriction (EC 50 ) was significantly less in the four to five-month-old male rats compared to the pooled data from older groups. Interestingly, four to five month old males had A61603 EC 50 values similar to the 8-to 12-month and 15+ old females. These studies conclude that an age related loss of sympathetic a-adrenergic constriction of renal interlobar arteries is present in Munich Wistar rats. Furthermore, this loss, while similar along longitudinal aspects of age, is also different as a function of gender with the loss of a-adrenergic constrictor function delayed in the female when compared to the male.

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Evidence for a noradrenergic innervation to α_1A‐adrenoceptors in rat kidney

Cited by 34 publications

References 12 publications

The contribution of adrenoceptor subtype(s) in the renal vasculature of diabetic spontaneously hypertensive rats

The contribution of adrenoceptor subtype(s) in the renal vasculature of diabetic spontaneously hypertensive rats

Existence of different α₁‐adrenoceptor subtypes in junctional and extrajunctional neurovascular regions in canine splenic arteries

Decreased alpha-adrenergic constriction of renal preglomerular arteries occurs with age and is gender-specific in the rat

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Evidence for a noradrenergic innervation to α1A‐adrenoceptors in rat kidney

Cited by 34 publications

References 12 publications

The contribution of adrenoceptor subtype(s) in the renal vasculature of diabetic spontaneously hypertensive rats

The contribution of adrenoceptor subtype(s) in the renal vasculature of diabetic spontaneously hypertensive rats

Existence of different α1‐adrenoceptor subtypes in junctional and extrajunctional neurovascular regions in canine splenic arteries

Decreased alpha-adrenergic constriction of renal preglomerular arteries occurs with age and is gender-specific in the rat

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Evidence for a noradrenergic innervation to α_1A‐adrenoceptors in rat kidney

Existence of different α₁‐adrenoceptor subtypes in junctional and extrajunctional neurovascular regions in canine splenic arteries