Drugs online research references
J Mol Cell Cardiol. 1994 Dec;26(12):1613-23.
Adenosine formation during hypoxia in isolated hearts: effect of adrenergic blockade.
Gorman MW, He MX, Sparks HV.
Department of Physiology, Michigan State University, East Lansing 48823.
Adrenergic receptor blockade has been reported to decrease cardiac adenosine formation and release during hypoxia. We wished to determine whether this occurs by an improvement in the energy supply/demand ratio. Isolated guinea pig hearts were perfused at a constant pressure of 50 mm Hg. Hypoxia (30% O2) was maintained for 20 min while adenosine release and venous PO2 were measured in the coronary venous effluent. beta-adrenergic blockade with 5 microM atenolol did not change hypoxic adenosine release (Control: 15.6 +/- 2.7, Atenolol: 23.6 +/- 5.7 nmol/g/20 min). Addition of 6 microM phentolamine with atenolol significantly reduced hypoxic adenosine release (4.4 +/- 1.4 nmol/g/20 min, P < 0.05). Atenolol was without hemodynamic effects, but addition of phentolamine reduced left ventricular pressure development, heart rate, and oxygen consumption prior to hypoxia. Atenolol plus phentolamine did not change venous PO2 during hypoxia. Treatment with phenoxybenzamine (1 microM) plus atenolol also reduced adenosine release (7.4 +/- 0.8 nmol/g/20 min). Control experiments and atenolol plus phentolamine experiments were repeated using 31P-NMR to measure high energy phosphates. Adrenergic blockade had no effect on phosphate concentrations during normoxia, but resulted in higher [PCr], lower [P(i)] and higher phosphorylation potentials during hypoxia. Adrenergic blockade also prevented the hypoxia-induced rise in intracellular [H+], [AMP] and [ADP] seen in control hearts. The changes in phosphorylation potential are correlated with similar changes in adenosine release in adrenergically intact hearts. We conclude that the primary effect of adrenergic blockade during hypoxia is a reduction in ATP use due to alpha-receptor blockade. This leads to improved high energy phosphate concentrations during hypoxia and a reduction in adenosine formation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7731056&dopt=Abstract
J Pharmacol Exp Ther. 1992 Dec;263(3):1253-60.
Involvement of adrenergic and angiotensinergic receptors in the paraventricular nucleus in the angiotensin II-induced vasopressin release.
Veltmar A, Culman J, Qadri F, Rascher W, Unger T.
Department of Pharmacology, University of Heidelberg, Germany.
The role of hypothalamic paraventricular adrenoceptors and angiotensin II (ANG II)-AT 1 receptors in mediating the vasopressin (AVP) release into the plasma in response to i.c.v. and local paraventricular ANG II injections was investigated in conscious chronically instrumented rats. Noradrenaline (NA) administered bilaterally into the paraventricular nucleus (PVN) dose-dependently stimulated AVP release. Bilateral PVN microinjections of the alpha 1 adrenoceptor agonists methoxamine and phenylephrine, or of the alpha2 adrenoceptor agonist clonidine, did not affect plasma AVP when given alone, but increased plasma AVP when methoxamine and clonidine were given in combination. In contrast, PVN microinjections of both the beta 1 adrenoceptor agonist dobutamine and the beta 2 adrenoceptor agonist salbutamol significantly reduced basal plasma AVP. Bilateral PVN pretreatment with the alpha 1 and alpha 2 adrenergic antagonists prazosin, idazoxan and rauwolscine, but not of the beta 1 and beta 2 adrenoceptor antagonists atenolol and ICI 118 551, significantly attenuated the i.c.v. ANG II-induced AVP release. ANG II injected bilaterally into the PVN dose-dependently increased plasma AVP. Bilateral PVN pretreatment with the specific ANG II-AT 1 receptor antagonist losartan partially inhibited the i.c.v. ANG II-induced AVP release. We conclude: 1) Beta 1 and beta 2 adrenoceptors in the PVN exert an inhibitory action on basal AVP secretion. 2) ANG II can release AVP by directly stimulating its ANG II-AT 1 receptors in the PVN. 3) PVN mediated AVP release in response to periventricular ANG II-AT 1 receptor stimulation is at least partially effected through ANG II-AT 1 receptors in the PVN impinging on alpha adrenergic terminals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1469631&dopt=Abstract
Drugs Exp Clin Res. 1986;12(5):393-6.
A comparison of the hypotensive and metabolic effects of 50 and 100 mg atenolol per day.
Lithell H, Aberg H, Selinus I.
Nine patients who had been treated for hypertension for many years with atenolol in a dose of 100 mg/day took part in this 18-month study, during which the dosage alternated between 50 and 100 mg/day for two-month periods. Blood pressure, heart rate, serum triglycerides and cholesterol and high density lipoprotein (HDL) lipids were checked at the end of each period. Altogether 27 and 32 measurements were made at the 50 and 100 mg dose levels respectively. Heart rate was lower by three beats/min (p less than 0.05) at the higher dose, but blood pressure and serum lipids and HDL cholesterol were not significantly different at the two dose levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3720523&dopt=Abstract
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