Modification of anti-hypertensive action of verapamil by inhibition of endogenous prostaglandin synthesis

Das, Undurti N.

doi:10.1016/0262-1746(82)90005-1

Cited by 12 publications

(3 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, besides any theoret ical consideration, our data suggest that nifedipine can be advantageously used in the treatment of hypertensive patients requiring treatment with NSAD. However, this statement cannot be generalized either to all NSAD or to all calcium entry blockers, considering that it has been reported that aspirin can reduce the antihypertensive effect of verapamil [26].…”

Section: Discussionmentioning

confidence: 99%

Calcium Antagonists: Interactions in Hypertension

et al. 1986

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Calcium Antagonists: Interactions in Hypertension

et al. 1986

View full text Add to dashboard Cite

“…Data have accumulated within the last few years suggesting that arachidonic acid metabolites may play a role in antihypertensive drug effects. The evidence for this is derived from animal experiments (Durao & Elvas 1979;Haeusler & Gerold 1979;Rubin & Lazar 1981;Hoffmann, Taube & Forster 1982;Maekawa, Liang & Hood 1982;Vemulapalli, Vander Vliet & Chiu 1982), single case reports (Das 1982) as well as from some clinical studies with hypertensive patients (Durao, Prata & Concalves 1977;Watkins et a1 1980, Abe eta/ 1980Moore eta/ 1981;Salvetti et a/ 1982;Mills et al 1982) and normal volunteers (Swartz et al 1980).…”

Section: Introductionmentioning

confidence: 99%

Influence of Prostaglandin Inhibition on Dihydralazine Induced Acute Effects in Patients With Essential Hypertension*

Heimann

Ratge

Wisser

et al. 1985

Clin Exp Pharma Physio

View full text Add to dashboard Cite

In order to determine whether vasodilator prostaglandins (PG) contribute to the acute vascular and endocrine responses to intravenously administered dihydralazine, we examined its effects on systolic and diastolic blood pressure (BP), heart rate (HR), plasma renin activity (PRA) and the plasma catecholamines (CA) noradrenaline (NA), adrenaline (A) and dopamine (DA) as well as on sodium, potassium and creatinine clearance (CNa, CK and CCr respectively), urinary flow rate, urinary catecholamines (NA, A, DA) and iPGE2 and i6-keto-PGF1 alpha excretion rate in six patients (three females, three males) with essential hypertension before and after PG synthesis inhibition by the nonsteroidal, anti-inflammatory agent diclofenac. Diclofenac, which reduced urinary iPGE2 and i6-keto-PGF1 alpha excretion by 62% (P = 0.026) and 45% (P = 0.037), respectively, antagonized dihydralazine induced diastolic BP reduction (P = 0.0009), HR increase (P = 0.01), noradrenaline and adrenaline increase in plasma (P = 0.02 and P = 0.05, respectively), increase in urine flow rate (P = 0.03), sodium clearance (P = 0.01) and tended to reduce PRA. We conclude that dihydralazine-mediated changes can be reduced by cyclo-oxygenase inhibition, most likely on the basis of a reduction of its effect on peripheral resistance, thereby leading to less reflex activation of the sympathetic nervous and renin-angiotensin systems.

show abstract

“…Antihypertensive effect of a calcium (Ca) antagonist, verapamil, has been shown to be inhibited by additional administration of aspirin, but to be unaffected by piroxicam (Das 1982;Baez et al 1987). Moreover, the antihypertensive effect of nifedipine was not affected by indomethacin (Salvetti et al 1986).…”

mentioning

confidence: 99%