• Publications
  • Influence
Pharmacological characterization of CGS 15943A: a novel nonxanthine adenosine antagonist.
TLDR
Results indicate that CGS 15943A antagonized both A1 and A2 receptor-mediated responses with a greater affinity toward the A2 than the A1 receptor subtype. Expand
Pharmacologic profile of CGS 24128, a potent, long-acting inhibitor of neutral endopeptidase 24.11.
TLDR
Thiorphan and CGS 24128 inhibited NEP in vitro with IC50 values of 5.0 +/-0.2 and 4.3 +/- 0.2 nM, respectively, and ANP-induced natriuresis was significantly potentiated in anesthetized rats pretreated with a bolus of CGS24128. Expand
Centrally mediated antihypertensive and bradycardic effects of methysergide in spontaneously hypertensive rats.
TLDR
Failure to identify a peripheral mechanism for the antihypertensive action of methysergide suggests that the effect may be centrally mediated but not reliant upon serotonin receptor blockade. Expand
Heterocyclic lactam derivatives as dual angiotensin converting enzyme and neutral endopeptidase 24.11 inhibitors.
TLDR
A series of 13- and 14-membered ring lactam derivatives 9a,b, 10, 11, and 12a-c was prepared from L-cysteine and showed dual plasma inhibition after intravenous or oral administration. Expand
Tachycardia in spontaneously hypertensive and normotensive rats after fusaric acid and bupicamide
1. The effects of the dopamine‐β‐hydroxylase inhibitors bupicamide, fusaric acid, FLA‐63 and U‐14,624 on blood pressure and heart rate of spontaneously hypertensive rats were examined.
Dual angiotensin converting enzyme/thromboxane synthase inhibitors.
TLDR
The blood pressure-lowering actions of enalapril were significantly potentiated by concurrent administration of 3, a thromboxane synthase inhibitor, and analysis of the area under the curve for 24 h showed nearly a doubling of the blood Pressure Lowering effect. Expand
Ontogenesis of hypertension and responsiveness to antihypertensive agents in spontaneously hypertensive rats.
TLDR
It is suggested that a progression of change in responsiveness to antihypertensive agents exists for SHR and this progression will differ for agents with differing mechanisms of action and is probably a result of physical and/or biochemical factors which combine to alter the responsivity of SHR vascular smooth muscle. Expand
Inhibition of thromboxane synthetase potentiates the antihypertensive action of an angiotensin-converting enzyme inhibitor by a prostaglandin-dependent but kinin-independent mechanism.
TLDR
Although the interaction between an ACEI and a TxSI is a prostaglandin-dependent mechanism, it is not mediated by endogenous kinins and may serve to explain the potentiation of the antihypertensive action of ACEI after inhibition of thromboxane synthetase. Expand