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Therapeutic Role of Calcium Antagonists in Essential Hypertension

  • A. E. Doyle

Summary

This meeting has focussed on a number of issues relevant to the definition of the optimal therapeutic role of calcium antagonists in the treatment of essential hypertension.

A major, and as yet unresolved, question is whether a disturbance of calcium transport mechanisms in vascular smooth muscle represents a fundamental fault in essential hypertension. To demonstrate that this is the case, disturbances of calcium transport and an associated vascular hyper-reactivity must be shown to precede the development of hypertension [1,2]. The study reported by Mulvany leaves this question unresolved, somewhat since although there was a hint of vascular hypersensitivity to the calcium ion in the young spontaneously hypertensive rats (SHR), his elegant genetic studies rather suggested that this change did not segregate with blood pressure in the F2 SHR-WKY hybrid animals. This finding must cast considerable doubt on the possible pathogenetic role of disturbances in the intravascular calcium ion in hypertension. The alternative is of course that structural change, and in particular hypertrophy of vascular smooth muscle occurring as a consequence of hypertension, might be responsible for the observed hyper-responsiveness to calcium and calcium antagonists in established hypertension both in man and in animals. The presence of such disturbances was clearly demonstrated in many of the papers presented at this meeting.

Even though the pathogenetic role of the calcium ion in essential hypertension is doubtful, there is little doubt that in essential hypertension calcium antagonists, whether dihydropyridine derivates, verapamil or diltiazem, are potent antihypertensive agents [3–5]. It now seems clear that the acute side effects of nifedipine, consisting of reflex tachycardia, headache, facial flushing and ankle oedema, are greatly reduced if a longer acting preparation is used. Nevertheless, the incidence of such side effects may be sufficiently high to limit somewhat the use of these derivates as first-line therapy in mild or moderate hypertension. They remain particularly valuable in combination with beta-blocking drugs [4].

Verapamil and diltiazem are substantially free of the characteristic side effects of the vasodilator dihydropyridines. They seem effective antihypertensive agents, particularly in mild hypertensives, and may be especially useful in patients with concomitant obstructive lung disease and diabetes, in whom beta-blocking drugs may be contraindicated. They are also effective drugs in the relief of angina.

This meeting has underlined the scientific basis of the use of drugs which block calcium transport and has emphasized the potential value of these drugs as therapeutic agents in the treatment of hypertension. There seems no doubt that the development of calcium antagonist drugs represents a major advance in the therapeutics of hypertension.

Keywords

Essential Hypertension Calcium Antagonist Calcium Transport Pathogenetic Role Ankle Oedema 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Aoki K, Ikeda N, Yamashita K, Tazumi K, Sato I, Hotta K (1974) Cardiovascualr contraction in spontaneously hypertensive rat: Ca2+ interaction of myofibrils and subcellular membrane of heart and arterial smooth muscle. Jpn Circ J 38:1115PubMedCrossRefGoogle Scholar
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    Aoki K, Asano M (1986) Effects of Bay k 8644 and nifedipine on femoral arteries of spontaneously hypertensive rats. Br J Pharmacol 88:221PubMedGoogle Scholar
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    Aoki K, Yoshida T, Kato S, Tazumi K, Sato I, Takikawa K, Hotta K (1976) Hypotensive action and increased plasma renin activity by Ca2+ antagonist (nifedipine) in hypertensive patients. Jpn Heart J 17:479PubMedCrossRefGoogle Scholar
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    Aoki K, Kondo S, Mochizuki A, Yoshida T, Kato S, Kato K, Takikawa K (1978) Antihypertensive effect of cardiovascular effect of cardiovascular Ca2+-antagonist in hypertensive patients in the absence and presence of beta-adrenergic blockade. Am Heart J 96:218PubMedCrossRefGoogle Scholar
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    Aoki K, Sato K, Kondo S, Yamamoto M (1983) Hypotensive effects of diltiazem to normals and essential hypertensives. Eur J Clin Pharmacol 25:475PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Tokyo 1986

Authors and Affiliations

  • A. E. Doyle
    • 1
  1. 1.Department of Medicine, Austin HospitalUniversity of MelbourneHeidelbergAustralia

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