PubMed · 6551244
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J C Hartshorn. Administering calcium-channel blocking agents.. https://doi.org/10.1097/00003465-198303000-00001
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BACKGROUND: We studied the participation of K(+) channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca(2+) channels on modulation of adrenergic responses by K(+) channels blockade. METHODS: Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. RESULTS: Iberiotoxin (10(-7) mol/L), an inhibitor of large conductance Ca(2+)-activated K(+) channels, and charybdotoxin (10(-7) mol/L), an inhibitor of both large and intermediate conductance Ca(2+)-activated K(+) channels, enhanced the contractions elicited by electrical field stimulation and produced a leftward shift of the concentration-response curve to norepinephrine. In contrast, the inhibitor of small conductance Ca(2+)-activated K(+) channels apamin (10(-6) mol/L) did not modify the contractile response to electrical field stimulation or norepinephrine. In the presence of the dihydropyridine Ca(2+)-channel blocker nifedipine (10(-6) mol/L), iberiotoxin and charybdotoxin failed to enhance the contractile responses to electrical field stimulation and norepinephrine. CONCLUSIONS: The results suggest that large conductance Ca(2+)-activated K(+) channels are activated by stimulation with norepinephrine to counteract the adrenergic-induced contractions of human saphenous vein. Thus, inhibition of these channels increases significantly the contraction, an effect that appears to be mediated by an increase in Ca(2+) entry through L-type voltage-dependent Ca(2+) channels.
Calcium antagonists have been shown to be superior over other antihypertensive drugs to prevent stroke. Because this cannot be fully attributed to blood pressure lowering effects, other mechanisms seem to play a role. Previously we found in patients with subarachnoid hemorrhage that nimodipine enhances fibrinolytic activity. The purpose of this systematic review was to investigate the fibrinolytic effect of calcium antagonists in general, especially in patients with hypertension. We systematically studied the entire PUBMED and EMBASE database with the search terms 'calcium antagonist' combined with 'fibrinolysis', '(euglobulin) clot lysis time' (ECLT), 'tissue plasminogen activator' (tPA), or 'plasminogen activator inhibitor' (PAI). Twenty-six prospective studies were identified and 22 manuscripts were included (802 investigated individuals). The results show that calcium antagonists significantly increase fibrinolysis as shown by a reduction of the ECLT standardized mean differences (SMD) -0.58 (95% confidence interval (CI) -1.05 to -0.11)) and an increase of tPA activity (SMD 0.73 (95% CI 0.25 to 1.21)). This increase of fibrinolysis is apparently caused by an increase of the tPA antigen level (SMD 0.16 (95% CI -0.05 to 0.37)) and a decrease of the plasminogen activator inhibitor-1 antigen antigen (SMD -0.36 (95% CI -0.74 to 0.02)). A sensitivity analysis showed that dihydropyridines, but not phenylalkylamines, exert a fibrinolytic effect. This fibrinolytic effect is not only seen in patients with subarachnoid hemorrhage but also in hypertensive patients. In conclusions, calcium antagonists increase fibrinolytic activity. This may add to the beneficial pharmacological effect of calcium antagonists to prevent ischemic events in patients with hypertension and subarachnoid hemorrhage.
BACKGROUND: Although the superior vena cava (SVC) may be involved in the triggering or maintenance of atrial fibrillation (AF), the electrophysiological properties of SVC in human are ill-defined. METHODS: The baseline effective refractory periods (ERPs) of high right atrium (HRA), SVC and the conduction time (CT) between HRA and SVC were measured at pacing cycle lengths (PCL) of 600 and 400 ms respectively in 20 patients (12 females, age 46+/-13 years) with paroxysmal supraventricular tachycardia. Immediately after acute electrical remodeling (ER) induced by constant HRA or SVC pacing at PCL of 400 ms for 5 min, ERPs of HRA, SVC and the CT between HRA and SVC were determined. After verapamil was administered, the same protocols for determining ERPs of HRA, SVC and the CT between HRA and SVC were repeated. RESULTS: The baseline ERP of SVC was significantly longer than that of HRA. The CT from SVC to HRA was significantly longer than that from HRA to SVC. After acute ER, both the ERPs of HRA and SVC were significantly shortened. However, no significant changes of the CT between HRA and SVC could be demonstrated. After verapamil infusion, significant shortening of the ERP of HRA and SVC still occurred following acute ER and the ERP of SVC was still longer than that of HRA. CONCLUSIONS: In human, ER can occur both in HRA and SVC after a short and moderately rapid heart rate pacing either from HRA or SVC. Verapamil cannot prevent such ER from occurring.