Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Nicholls, D. P.; Harron, D. W. G.; Shanks, R. G.

doi:10.1111/j.1365-2125.1983.tb01458.x

Cited by 10 publications

(8 citation statements)

References 26 publications

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“…These results are similar to those reported in a previous study, in which labetalol reduced arterial pressure in normal man in the sitting position, with no change in heart rate (Richards et al, 1974). The present study also confirms that alinidine reduces systolic and diastolic arterial pressure in the supine and standing positions, and that these reductions are accompanied by small reductions in heart rate (Harron et al, 1982a;Nicholls et al, 1983b). Plasma NA is derived from the sympathetic nervous system, and the concentration is therefore determined by the rate of NA release in the synaptic cleft, its local uptake and metabolism, the degree of spillover into the circulation and the peripheral plasma clearance of NA.…”

Section: Discussionsupporting

confidence: 93%

“…Labetalol reduces arterial pressure in man through aadrenoceptor blockade, and the reduction is not accompanied by an increase in heart rate, as the reflex tachycardia is prevented by concomitant 1-adrenoceptor blockade (Boakes et al, 1971;Richards et al, 1974;. Alinidine reduces arterial pressure in normal man by an unknown mechanism (Harron et al, 1982a;Nicholls et al, 1983b) and reduces heart rate by a direct action on the sino-atrial node (Kobinger et al, 1979a, b).…”

Section: Introductionmentioning

confidence: 99%

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Effect of indoramin, labetalol and alinidine on sympathetic function in normal man.

Nicholls¹,

McNeill²,

O'Connor³

et al. 1984

Brit J Clinical Pharma

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1 The effects of single oral doses of indoramin (mean dose 58 mg), labetalol (mean dose 150 mg), alinidine 80 mg and placebo on arterial pressure and heart rate in the supine and standing positions were studied in six normal volunteers. Doses were chosen to give equivalent reductions of arterial pressure in the standing position. Observations were made before and at 2 and 4 h after drug administration.2 Plasma noradrenaline (NA) was measured at each time interval in the supine position, and after 4 min of standing. Plasma renin activity (PRA) was measured at each time interval after 30 min in the standing position. 3 In the supine position, alinidine produced a significant reduction of systolic arterial pressure from 124.0 + 3.0 mm Hg to 104.3 + 4.1 mm Hg at 2 h (P < 0.01) and to 101.7 ± 2.2 mm Hg at 4 h (P < 0.01). Diastolic pressure was reduced from 74.7 ± 2.6 mm Hg to 57.0 + 4.6 mm Hg at 4 h (P < 0.01). Arterial pressure was unchanged after indoramin or labetalol administration. 4 In the supine position, heart rate was unchanged after indoramin, and small reductions were observed after labetalol and alinidine. Indoramin produced a significant increase in plasma NA. A small increase of plasma NA was observed after labetalol, and a small decrease after alinidine. 5 In the standing position, the three active drugs reduced systolic arterial pressure to a similar extent (indoramin, -26.7 mm Hg at 4 h after drug administration; labetalol, -21.3 mm Hg at 2 h; alinidine, -21.7 mm Hg at 4 h). 6 In the standing position, heart rate was increased by indoramin (+6.6 beats min-' at the time of maximum arterial pressure reduction) but reduced by labetalol (-10.4 beats min-') and alinidine (-7.6 beats min-). Plasma NA was increased after indoramin and labetalol (+ 191 and + 137 pg ml-1 respectively) but a small reduction was observed after alinidine (-128 pg ml-'). PRA was unchanged after labetalol. A small increase of PRA was observed after indoramin, and a significant increase after alinidine administration (1.29 ± 0.16 to 2.32 + 0.44 ng angiotensin I ml-' h-1 at 2 h, P < 0.05). 7 The effects of indoramin and labetalol may be correlated with their known pharmacological properties. Alinidine produced small reductions of heart rate and plasma NA, and an increase of PRA. The mechanism of the hypotensive action of alinidine is unknown, but these results suggest the possibility that reduction of sympathetic activity may be a component of this action.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Effect of indoramin, labetalol and alinidine on sympathetic function in normal man.

Nicholls¹,

McNeill²,

O'Connor³

et al. 1984

Brit J Clinical Pharma

Self Cite

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“…Because of its bradycardic activity, alin idine has often been compared to beta block ers [9,13,14]. Improvement in exercise tol erance, rate-pressure product and time to ischemic threshold achieved by alinidine treatment were not different from those in duced by beta adrenergic blockers.…”

Section: Discussionmentioning

confidence: 99%

“…A reduction in heart rate has been shown in healthy subjects [23], in patients with sinus tachycardia due to treatment with catechol amines and vasodilators [9], in patients with hyperkinetic heart syndrome [23], emotion ally induced tachycardia [ 10], myocardial in farction [7,24,26], cardiogenic shock [26] and during neuroleptanesthesia [25]. This decrease in sinus rate is not achieved by inhi bition or activation of the autonomic ner vous system and its neurotransmitter sub stance and receptors, but by means of a direct action on pacemaker cells of the sinoa trial node [1][2][3][4]6].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, negative inotropic properties independent of changes in heart rate have been reported [7,8]. However, this drug reduces standing and supine rest heart rate and more markedly exercise [9] or emotional tachycardia [10]. Since heart rate is a major determinant of myocardial oxygen consump tion [11], in patients with effort angina this effect allows for an improved exercise toler ance [12][13][14][15], An abnormal shortening of diastolic time has been shown during exercise in patients with coronary artery disease [15,16], Dia stolic duration being an important determi nant of myocardial perfusion [17], this phe nomenon may play a role in worsening exer cise-induced ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Alinidine in Chronic Stable Angina: The Effect on Diastolic Perfusion Time

et al. 1990

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The present study has been performed to assess the effects of alinidine on diastolic duration during exercise in chronic coronary artery disease. Twelve male patients with stable effort angina and without previous myocardial infarction were studied. They received alinidine or placebo in a double-blind randomized crossover trial for 3 days after a wash-out period of 4 days. Alinidine was administered at a dosage of 30 mg 3 times a day. At the end of each treatment the patients underwent upright bicycle exercise. Left ventricular time intervals were obtained by means of carotid thermistor plethysmography. Diastolic duration was calculated by subtracting the electromechanical systole from the R-R interval and expressed as a percentage of the cardiac cycle (%D). Alinidine increased both total exercise duration from 246.7 ± 120.7 to 346.6 ± 114.1 s (p < 0.05) and time to 0.1-mV ST segment depression from 98.3 ± 53 to 187.2 ± 105 s (p < 0.05). Similarly the drug induced a reduction of the rate-pressure product and of the extent of ischemic ST segment depression during exercise. %D was increased by alinidine both at rest and during exercise. A direct linear regression between R-R and %D was found after both alinidine and placebo treatments either at rest or during exercise. Nevertheless, no difference was observed between both slopes and intercepts. Therefore, since the relationship between R-R interval and %D was unaffected by alinidine, it was possible to hypothesize that the changes in diastolic duration were due only to the bradycardic action of the drug.

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Deciphering the sinus tachycardias

Yusuf

Camm

2005

Clin Cardiol

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Summary: Sinus tachycardia is the most common rhythm disturbance encountered in clinical practice. Primary sinus tachycardia without an underlying secondary cause, despite often being associated with troublesome symptoms, is often neglected leading to multiple consultations and frustration on part of both the practitioner and the patient. The fact that primary sinus tachycardias are a heterogeneous group of disorders is seldom appreciated; hence, a firm diagnosis is rarely reached and management is haphazard. Furthermore, there may be prognostic implications for prolonged or recurrent sinus tachycardia, making it imperative that this group of arrhythmias receive adequate and appropriate attention. Normal sinus tachycardia (i.e., secondary), inappropriate sinus tachycardia, postural orthostatic tachycardia syndrome (POTS) and sinus node reentry tachycardia make up this group of arrhythmias. Their definitions, clinical features, diagnostic criteria, pathophysiologic mechanisms, and optimum management are discussed in this review.

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Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Cited by 10 publications

References 26 publications

Effect of indoramin, labetalol and alinidine on sympathetic function in normal man.

Effect of indoramin, labetalol and alinidine on sympathetic function in normal man.

Alinidine in Chronic Stable Angina: The Effect on Diastolic Perfusion Time

Deciphering the sinus tachycardias

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