Drugs online research references
Brain Res. 1987 Sep 22;421(1-2):226-34.
Parabrachial lesions increase plasma norepinephrine concentration, plasma renin activity and enhance baroreflex sensitivity in the conscious rat.
Hubbard JW, Buchholz RA, Keeton TK, Nathan MA.
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764.
Electrolytic lesions of the parabrachial nucleus (PBN) caused significant increases in basal plasma renin activity (+433%) and basal plasma norepinephrine concentration (+98%) in conscious rats. Plasma epinephrine concentration, mean arterial pressure, heart rate, hematocrit, plasma osmolality and plasma sodium and potassium concentrations were not significantly affected by the lesions. Atenolol reduced the elevated plasma renin activity in the lesion group to a value similar to that of a control group (sham lesions or lesions in areas adjacent to the PBN). Captopril significantly lowered mean arterial pressure in the lesion group, but it had no effect on arterial pressure in the control group. Lesions of the PBN also increased the baroreflex-mediated bradycardia evoked by an abrupt elevation of arterial pressure. We propose that the PBN tonically inhibits sympathetic activity, sympathetically mediated renin release and baroreflex sensitivity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3319038&dopt=Abstract
Can J Physiol Pharmacol. 1997 Jul;75(7):763-71.
Vasoconstrictor-mediated increase in muscle resting thermogenesis is inhibited by membrane-stabilizing agents.
Tong AC, Rattigan S, Dora KA, Clark MG.
Division of Biochemistry, University of Tasmania, Hobart, Australia.
Norepinephrine and angiotensin II are potent vasoconstrictors and stimulate thermogenesis (oxygen uptake) as well as lactate and glycerol efflux in the constant-flow perfused rat hind limb at rest. However, the mechanism by which oxygen uptake (VO2) is increased is unknown, and it is not clear whether vasoconstriction is required for the increase in VO2 by the hind limb. In the present study the association between vasoconstriction and VO2 was further investigated, and a chance observation that high-dose propranolol selectively blocked vasoconstrictor-induced increase in VO2 was further explored. The norepinephrine-mediated increase in VO2 was totally blocked by either 50 microM (+)-propranolol or 50 microM (-)-propranolol (active beta-blocking enantiomer), but only (+)-propranolol reduced the vasoconstriction. Similarly, 100 microM (+/-)-propranolol (a dose likely to cause plasma membrane stabilizing effects involving interruption and (or) prevention of action potentials) blocked increases in VO2, lactate, and glycerol efflux by 5 nM angiotensin II (a nonadrenergic vasoconstrictor) with only marginal effects on pressure development. (+/-)-Propranolol (100 microM) had no effect on postequilibration red blood cell washout mediated by angiotensin II, a putative indicator of vasoconstrictor-induced redistribution of flow. Quinidine (260 microM) (an antiarrhythmic agent with membrane-stabilizing activity) inhibited only the increase in VO2, but neither nadolol (300 microM) nor atenolol (300 microM) (beta-blockers without membrane-stabilizing activity) inhibited VO2 or perfusion pressure increases produced by 5 nM angiotensin II. Veratridine (a membrane labilizer that is capable of evoking plasma membrane depolarization by maintaining voltage-gated Na+ channels in their open state) increased VO2 without vasoconstriction, and the increase in VO2 was blocked by 100 microM (+/-)-propranolol. It is concluded that the increase in hind-limb VO2 results from a destabilization of skeletal muscle plasma membranes. This can be achieved directly by veratridine or indirectly by angiotensin II, involving vasoconstriction and redistribution of flow. The findings suggest a novel mechanism for resting muscle thermogenesis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9315342&dopt=Abstract
Br J Clin Pharmacol. 1984;17 Suppl 1:108S-111S.
The influence of indomethacin and sulindac on some pharmacological actions of atenolol in hypertensive patients.
Salvetti A, Pedrinelli R, Alberici P, Magagna A, Abdel-Haq B.
Indomethacin and sulindac were used as tools to study the role of renal and/or systemic prostaglandins in the pharmacological response to atenolol. Patients receiving chronic treatment with atenolol 100 mg received indomethacin 50 mg twice daily or sulindac 200 mg twice daily in a randomised crossover trial. Indomethacin significantly reduced the antihypertensive action of atenolol while sulindac had no effect. The role that systemic and/or renal prostaglandins may play in the antihypertensive action of atenolol is discussed with reference to renal PGI2 production and inhibition of platelet cyclo-oxygenase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6378233&dopt=Abstract
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