Pharmacological characterization and anatomical localization of prejunctional β‐adrenoceptors in the rat kidney

Lakhlani, Parul P.; Amenta, Francesco; Napoleone, Paolo; Felici, Laura; Eikenburg, Douglas C.

doi:10.1111/j.1476-5381.1994.tb14886.x

Cited by 5 publications

(8 citation statements)

References 46 publications

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“…On the other hand, it still remains controversial whether all β-adrenoceptor blockers have a prophylactic efficacy in migraine or it is limited to individual members of this drug class with specific characteristics. β-blockade results in (a) inhibition of noradrenaline release by blocking prejunctiononal β-adrenoceptors (Lakhlani et al 1994) and (b) a delayed reduction in tyrosine hydroxylase activity, the rate-limiting step in noradrenaline synthesis, in the superior cervical ganglia (Hieble 2000). It is also suggested that lipophilicity (penetration into the central nervous system), membrane-stabilizing effects and intrinsic sympathomimetic activity are relevant for antimigraine efficacy.…”

Section: β-Adrenoceptorsmentioning

confidence: 99%

Current and prospective pharmacological targets in relation to antimigraine action

Mehrotra

Gupta

Chan

et al. 2008

Naunyn-Schmied Arch Pharmacol

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Migraine is a recurrent incapacitating neurovascular disorder characterized by unilateral and throbbing headaches associated with photophobia, phonophobia, nausea, and vomiting. Current specific drugs used in the acute treatment of migraine interact with vascular receptors, a fact that has raised concerns about their cardiovascular safety. In the past, α-adrenoceptor agonists (ergotamine, dihydroergotamine, isometheptene) were used. The last two decades have witnessed the advent of 5-HT 1B/1D receptor agonists (sumatriptan and second-generation triptans), which have a well-established efficacy in the acute treatment of migraine. Moreover, current prophylactic treatments of migraine include 5-HT 2 receptor antagonists, Ca 2+ channel blockers, and β-adrenoceptor antagonists. Despite the progress in migraine research and in view of its complex etiology, this disease still remains underdiagnosed, and available therapies are underused. In this review, we have discussed pharmacological targets in migraine, with special emphasis on compounds acting on 5-HT (5-HT 1-7 ), adrenergic (α 1 , α 2, and β), calcitonin gene-related peptide (CGRP 1 and CGRP 2 ), adenosine (A 1 , A 2 , and A 3 ), glutamate (NMDA, AMPA, kainate, and metabotropic), dopamine, endothelin, and female hormone (estrogen and progesterone) receptors. In addition, we have considered some other targets, including gamma-aminobutyric acid, angiotensin, bradykinin, histamine, and ionotropic receptors, in relation to antimigraine therapy. Finally, the cardiovascular safety of current and prospective antimigraine therapies is touched upon.

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Section: β-Adrenoceptorsmentioning

confidence: 99%

Current and prospective pharmacological targets in relation to antimigraine action

Mehrotra

Gupta

Chan

et al. 2008

Naunyn-Schmied Arch Pharmacol

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“…, 1977; Vanter et al. , 1985) and there is convincing evidence that both β 1 ‐ and β 2 ‐adrenoceptors are present in the renal vasculature (Lakhlani et al. , 1994).…”

Section: Introductionmentioning

confidence: 99%

“…, 2001). Studies of the anatomical localization of β‐adrenoceptor subtypes mediating facilitation of stimulus‐induced overflow of noradrenaline have suggested the presence of a homogeneous population of prejunctional β 2 ‐adrenoceptors (Lakhlani et al. , 1994).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Ang II and renal sympathetic nerve influence dopamine‐and isoprenaline‐induced renal haemodynamic changes in normal Wistar–Kyoto and spontaneously hypertensive rats

Abdulla

Sattar

Abdullah

et al. 2008

Auton Autocoid Pharmacol

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1. This study was undertaken to elucidate the effects of inhibiting the renin-angiotensin system (RAS) with losartan, and acute unilateral renal denervation on renal haemodynamic responses to intrarenal administration of vasoconstrictor doses of dopamine and vasodilator doses of isoprenaline in Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). 2. Acute unilateral renal denervation of the left kidney in rats was confirmed by a drop in the renal vasoconstrictor response to renal nerve stimulation (P < 0.05) along with diuresis and natriuresis. Rats were pretreated with losartan for 7 days and thereafter animals fasted overnight were anaesthetized (sodium pentobarbitone, 60 mg/kg i.p.) and acute renal haemodynamic responses studied. 3. Dose-response curves were constructed for dopamine and isoprenaline that induced falls or increases in renal blood flow, respectively. It was observed that renal vascular responses were greater in the denervated as compared with rats with intact renal nerves (all P < 0.05). Dopamine-induced renal vasoconstrictor responses were markedly lower in losartan-treated denervated WKY and SHR compared with their untreated counterparts (all P < 0.05). It was also observed that in losartan-treated and denervated WKY rats the vasodilatory responses to isoprenaline were markedly lower compared with untreated rats (all P < 0.05). However, in SHR, under the same conditions, there was no difference in the renal response to isoprenaline whether or not rats were treated with losartan (P > 0.05). 4. The data obtained showed that the renal vasoconstrictor effect of dopamine depends on intact renal nerves and RAS in WKY and SHR. Isoprenaline responses were likewise sensitive to renal denervation and RAS inhibition in WKY rats but not SHRs. Our observations reveal a possible relationship between renal AT(1) receptors and alpha(1)-adrenoceptors in WKY and SHR. There is also evidence to suggest an interaction between renal beta-adrenoceptors and AT(1) receptors in WKY rats.

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“…Ten animals were anesthetized with an IP injection of pentobarbital sodium (60 mg/kg) and laparotomized. The right renal artery was exposed and denervated by stripping the artery surgically and swabbing it with a 10% phenol solution dissolved in ethanol according to the procedure detailed elsewhere (Lakhlani et al 1994). The remaining rats were sham-operated.…”

Section: Animals and Tissue Treatmentmentioning

confidence: 99%

“…NE was assayed by high-pressure liquid chromatography (HPLC) with electrochemical detection (Lakhlani et al 1994). …”

Section: Ne Assaymentioning

confidence: 99%

Dopamine D4 Receptor Expression in Rat Kidney: Evidence for Pre- and Postjunctional Localization

Rícci

Marchal-Victorion

Bronzetti

et al. 2002

J Histochem Cytochem.

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S U M M A R Y Dopamine D4 receptors mediate inhibition of vasopressin-dependent sodium reabsorption by dopamine in collecting tubules. At present, the distribution of D4 receptors in other renal districts remains an open issue. The renal distribution of D4 receptor was assessed in normally innervated and denervated male Sprague-Dawley rats by quantitative immunohistochemistry using an anti-dopamine D4 receptor rabbit polyclonal antibody. D4 receptor protein immunoreactivity was observed perivascularly in the adventitia and the adventitia-media border. The density of perivascular dopamine D4 receptor was higher in afferent and efferent arterioles than in other segments of the renal vascular tree. Renal denervation abolished perivascular dopamine D4 receptor protein immunoreactivity. In renal tubules, the epithelium of collecting tubules showed the highest dopamine D4 receptor protein immunoreactivity, followed by the epithelium of proximal and distal tubules. No dopamine D4 receptor protein immunoreactivity was observed in the epithelium of the loop of Henle. Denervation did not change dopamine D4 receptor protein immunoreactivity in renal tubules. These results indicate that rat kidney expresses dopamine D4 receptors located both prejunctionally and nonprejunctionally in collecting, proximal, and distal tubules. This suggests that the dopamine D4 receptor may be involved in the control of neurotransmitter release and in renal hemodynamic and tubule function.

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Pharmacological characterization and anatomical localization of prejunctional β‐adrenoceptors in the rat kidney

Cited by 5 publications

References 46 publications

Current and prospective pharmacological targets in relation to antimigraine action

Current and prospective pharmacological targets in relation to antimigraine action

Inhibition of Ang II and renal sympathetic nerve influence dopamine‐and isoprenaline‐induced renal haemodynamic changes in normal Wistar–Kyoto and spontaneously hypertensive rats

Dopamine D4 Receptor Expression in Rat Kidney: Evidence for Pre- and Postjunctional Localization

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