Purine agonists prevent trophic changes caused by sympathetic denervation

Albino‐Teixeira, António; Azevedo, Isabel; Branco, D.; Osswald, Walter

doi:10.1016/0014-2999(90)90411-x

Cited by 24 publications

(10 citation statements)

References 35 publications

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“…However, 6-9 weeks after pelvic ganglion removal, the adrenergic innervation had reappeared, although the origin of the regenerating fibres was not resolved. Studies on the vascular system show that P1 receptor agonists prevent the trophic changes caused by sympathetic denervation, which was taken to be consistent with an involvement of purines in the trophic effects of sympathetic innervation [13]. In spontaneously hypertensive rats, where there is increased sympathetic nerve activity, there is hyperactive bladder voiding that appears to be associated with higher secretion of NGF by bladder smooth muscle and hyperinnervation [156,633].…”

Section: Changes Due To Selective Denervationmentioning

confidence: 89%

Purinergic signalling in the urinary tract in health and disease

Burnstock

2013

Purinergic Signalling

140

149

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Purinergic signalling is involved in a number of physiological and pathophysiological activities in the lower urinary tract. In the bladder of laboratory animals there is parasympathetic excitatory cotransmission with the purinergic and cholinergic components being approximately equal, acting via P2X1 and muscarinic receptors, respectively. Purinergic mechanosensory transduction occurs where ATP, released from urothelial cells during distension of bladder and ureter, acts on P2X3 and P2X2/3 receptors on suburothelial sensory nerves to initiate the voiding reflex, via low threshold fibres, and nociception, via high threshold fibres. In human bladder t h e p u r i n e rg i c c o m p o n e n t o f p a r a s y m p a t h e t i c cotransmission is less than 3 %, but in pathological conditions, such as interstitial cystitis, obstructed and neuropathic bladder, the purinergic component is increased to 40 %. Other pathological conditions of the bladder have been shown to involve purinoceptor-mediated activities, including multiple sclerosis, ischaemia, diabetes, cancer and bacterial infections. In the ureter, P2X7 receptors have been implicated in inflammation and fibrosis. Purinergic therapeutic strategies are being explored that hopefully will be developed and bring benefit and relief to many patients with urinary tract disorders.

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Section: Changes Due To Selective Denervationmentioning

confidence: 89%

Purinergic signalling in the urinary tract in health and disease

Burnstock

2013

Purinergic Signalling

140

149

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“…This is also the case for a more indirect role of the periarterial innervation. Auto nomic nerves seem to promote the differentiation of arterial smooth muscle cells [39][40][41] possibly including key features of the postjunctional growth response to All. Of interest in this respect is the balance between ATI and AT2 receptors which have recently been proposed to stim ulate and inhibit arterial smooth muscle growth, respec tively [30], and receptor-mediated internalization of All, which seems to be essential at least for renal structural changes [42], Future analyses of arterial All content and AT receptor expression in conjunction with All infusion and sympatholytic interventions may help to dissociate between these possibilities.…”

Section: Other Types O F Arteriesmentioning

confidence: 99%

Angiotensin II Induces Media Hypertrophy and Hyperreactivity in Mesenteric but Not Epigastric Small Arteries of the Rat

et al. 1997

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We examined effects of a 2-week infusion of angiotensin II (All, 250 ng· kg^-1•min^-1) on properties of mesenteric resistance arteries (MrA) and superior epigastric arteries (SEA) of male Wistar rats. Histochemistry and pharmacological tools showed that MrA are densely innervated, whereas SEA are only sparsely innervated. All infusion resulted in a significant elevation in mean arterial pressure and in plasma All and noradrenaline levels. Organ chamber studies and morphometry were used to determine arterial contractile reactivity and structure. After All infusion, in MrA (i) maximal contractile responses to 125 mM K⁺, noradrenaline, serotonin and adrenergic nerve stimulation were significantly increased, without modification of the sensitivity to these stimuli and (ii) a significant increase in media cross-sectional area and media thickness was observed without alterations in lumen diameter. The observed increase in vascular reactivity could fully be attributed to the observed increase in wall mass since no alterations in maximal active wall stress were noted. In SEA, no significant changes in responsiveness to vasoconstrictor stimuli or in wall structure were observed. These findings suggest that perivascular nerves are involved in the hypertrophy and subsequent hyperreactivity of small arteries in rats exposed for 2 weeks to a low dose of AII

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“…Adenosine is an important modulator of the cardiovascular system and its actions include vasodilation, modulation of sympathetic activity (Albino‐Teixeira, Azevedo, Branco & Osswald, 1990a) and inhibition of renin release thus regulating the renin–angiotensin system (Tagawa & Vander, 1970; Osswald, Schmitz & Kemper, 1978; Spielman & Thompson, 1982; Kuan, Wells & Jackson, 1990; Jackson, 1991). The blockade of adenosine receptors with DPSPX leads to activation of the renin–angiotensin system.…”

Section: Introductionmentioning

confidence: 99%

Losartan and atenolol on hypertension induced by adenosine receptor blockade

Morato

Sousa

Guimarães

et al. 2003

Auton Autocoid Pharmacol

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1. The prolonged infusion of 1,3-dipropyl-8-sulfophenylxanthine (DPSPX), a non-selective antagonist of adenosine receptors, induces hypertension, an increase in plasma renin activity and morphological cardiovascular changes. 2. The aim of this work was to evaluate the effects of losartan, a selective AT1 receptor antagonist, and atenolol, a beta-adrenoceptor antagonist, on DPSPX-induced hypertension. 3. Male Wistar rats (250-300 g, n = 4-6) were treated for 1 or 4 weeks with: saline i.p.; DPSPX (90 microg kg(-1) h(-1)) i.p.; losartan (15 mg kg(-1) day(-1)) p.o.; atenolol (25 mg kg(-1) day(-1)) p.o.; DPSPX (90 microg kg(-1) h(-1)) i.p. + losartan (15 mg kg(-1) day(-1)) p.o.; DPSPX (90 microg kg(-1) h(-1)) i.p. + atenolol (25 mg kg(-1) day(-1)) p.o. Blood pressure was measured by the 'tail-cuff' method in conscious animals. Fragments of the mesenteric and tail arteries were processed for morphological study and the mean diameter of the vascular smooth muscle cells was determined. 4. DPSPX increased blood pressure. Losartan and atenolol prevented this rise but had no effect on blood pressure of control rats. DPSPX-treated groups showed hypertrophy of the vascular smooth muscle cells and proliferation of subintimal cells. Losartan but not atenolol prevented these changes. Losartan had no effect on the vascular morphology of control rats, while treatment with atenolol for 4 weeks induced hypertrophy of the vascular smooth muscle cells. 5. Both losartan and atenolol counteract the development of DPSPX-induced hypertension but only losartan prevents the alterations in vascular morphology.

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Purine agonists prevent trophic changes caused by sympathetic denervation

Cited by 24 publications

References 35 publications

Purinergic signalling in the urinary tract in health and disease

Purinergic signalling in the urinary tract in health and disease

Angiotensin II Induces Media Hypertrophy and Hyperreactivity in Mesenteric but Not Epigastric Small Arteries of the Rat

Losartan and atenolol on hypertension induced by adenosine receptor blockade

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