Hypertension Falls to Pressure from Nifedipine Oral nifediplne lowers BP In sever. hypertension .•.

In an open study, 19 patients (13 White, 4 Black and 2 Asian) with severe hypertension swallowed the contents of a lOmg capsule of nifedipine. Ten patients required a second dose 3().6() min later because theif mean arterial pressure had not decreased by 15%. Mean arterial pressure was significantly reduced between 10 and 240 min after drug ingestion. Further, BP was reduced from a mean baseline value of 187/122mm Hg to a mean of 149J92mm Hg at 120 min. Similarly. systemic vascular resistance was reduced significantly between 20 and 120 min (by 798 and 610 dynes/ sec/cm-5, respectively) . The mean heart rale was significantly increased from 82.8 beats/min at baseline to > 90 beats/min at 20, 30 and 60 min. Cardiac output also increased but the increase was signifICant only at 20 min.

No side effects were reported but there was a significant increase in the average urine level at 4 hours and a non·significant increase in the plasma renin concentration at 240 min. In conclusion, nifedipine was effective in reducing BP in patients with severe hypertension and did not cause neurological symptoms or hypotension. 0evidS<n. R.c.; Blnlen. S.L; Keeey, P A ; KfMy. M.A .00 Stewart, D.K.: ~ JoumaI of ~ 79 (Suppl . .fA): 26...11 (Oct 1985)

..• and in mUd to moderate hypertension when given alone or with labetalol ... After a 4-week placebo run·in, 25 patients with mild to moderate hypertension (WHO grades HI) were

randomly allocated in double·blind fashion, to 6 weeks' treatment with nifedipine 20mg bid or labetalol 200mg bid. II necessary, the dose was doubted in the second 2 weeks to achieve a diastolic BP .:!iO 90mm Hg. After a 2-week washout, the patients were crossed over to the alternate treatment. The trial ended with a 4-week period during which patients received niledipine + labetalol.

There was a significant decrease in mean supine BP of 4/3mm Hg in patients receiving niledipine and 8/4mm Hg in those taking labetalOl. There was a further reduction in BP with the combination therapy and this was significant compared with both drugs alone.The therapeutic goal (a diastolic BP .:!iO 90mm Hg) was reached in 16 patients receiving labetalol alone, 9 on nifedipine alone and in 21/23 given the combination. The standing heart rate was significantly increased in patients receiving niledipine while the standing and supine heart rate was decreased in those taking labetaJol. Nifedipine stimulated the renin-angiotensin-aldosterone system, labetalol inhibited it, and the combination caused no appreciable effects .

Seven patients receiving labetalol and 3 receiving the combination experienced dizzjness; 3 and 6 patients, respectively, had muscular weakness and fatigue as did 2 patients receiving nifedipine. Two patients receiving nifedipine also experienced flushing. There were no clinically significant changes in lipid or glucose metabolism apart from 1 patient who init ially had a slightly elevated fasting blood glucose. It was concluded that 'the cornbkldon of the drug_ con_titutes 8 rematkably _"fICtive entihypertenaNe regimen', o-.m.n, KP. Weiner, t .: l'Otl Schenck. H. and KartbetfI, B.E.: Europ6IIf! Journal of CInicaJ Pr!armacology 29: /49-154 (No 2. /985)

.. _ and it is effective for up to 2 years in patients with hypertension and renal disease .•• In an open study, 18 patients with persistent arterial hypertension (including 7 with hypertensive crises)

and chronic renal disease received a single oral dose of niledipine 10mg. Patients not responding were then given nifedipine 2Omg. Six patients subsequently received nifedipine 3O-4Omg and propranolol l 00-200mg intermittently for 2 years.

BP was significantly reduced within 5 min of single-dose nifedipine administration and this reduction was greatest at 25-30 min. The BP was stabilised within 'normal limits ' in the patients receiving 2 years' treatment with nifedipine and propranolol. During single-dose therapy, all patients experienced tachycardia, but this was lessened by concurrent therapy with propranolol. In addition, 7 patients reported dizziness, flushing and epigastric pain. Moten, J.: Barala. J,D ana ()I;a$. J.: NephroIl.fl : 31 .. -319 (Dec 1965)

, .• and sublingual nifedlpine rapidly controls hypertenSive cri. es In an open study, 30 patients with hypertensive emergencies (diastolic BP ;;1!: l20mm Hg or a systolic BP ~

190mm Hg with evidence of acute end organ dysfunction) were randomly allocated to receive sublingual nifedipine 10mg or 2Omg. If required, patients were given further doses of nifedipine (up to a maximum of 3Omg) and another antihypertensive.

Mean arterial pressure and BP decreased significantly within 5 min and the decreases in systolic (47mm Hg), diastolic (28mm Hg) and mean arterial pressures (36mm Hg) were greatest 35 min after drug administration. At 60 min, 97% of patients had a diastolic BP < 120mm Hg and 67% a diastolic BP < 100mm Hg. Four of the 11 patients receiving nifedipine 10mg and 2/19 receiving 20mg had an inadequate response initially and required a further 10mg of nifedipine. 14 patients required additional antihypertensive drugs. The results showed significant positive correlations between the decline in systolic and diastolic BP and the pretreatment BP. Four patients with cerebrovascular accidents died in hospital, and a fifth patient died 3 months later Irom unrelated causes.

During treatment, 1 patient experienced flushing, and another had a worsening of neurological symptoms which was later attributed to a slroke·in·evolulion. It was concluded that sublingual nifedipine was effective in the treatment of hypertensive emergencies and has high tolerability and a rapid onset of action. E~1. AG . Au/I. '10.; RJedinfIM. AI.S II1d Muratl. G.H . AmericMf JourNI of ~ 79 (Suppl. tlA): '9-25 (Oc' t985)

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