The rationality or irrationality of ganglion blocking agents in hypertension / by W.D.M. Paton.

  • Paton, William D. M.
Date:
[1959?]
Catalogue details

Licence: In copyright

Credit: The rationality or irrationality of ganglion blocking agents in hypertension / by W.D.M. Paton. Source: Wellcome Collection.

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    by others, that blood pressure is a unimodally distributed quantity: that, in other words, hypertensives are the right-hand tail of a distribution curve. This means that, for its pathogenesis, we must look for a cause which is both common and an extension of normal processes. What common, normal hy¬ pertensions are there? As far as I know, those mediated by the autonomic in so-called “stressful” situations are the only examples one can quote. If our everyday life is made up of fluctuations in blood pressure in response to circumstance, it seems perfectly reasonable to suppose that sometimes these fluctuations may become more prolonged and more persistent than usual. To look further for a primary cause of hypertension seems rather like trying to explain the popularity of pin-up girls, not by the attractiveness of the girls portrayed, but on a theory, say, that young men like hammering tacks into walls! 4. The fourth argument one can advance is that the whole picture of hypertension is interpretable by taking a neurogenic starting-point. By this I mean that if one postulates an initial autonomic activity, one can then readily suppose that in due course the blood vessels, through their exposure to a higher hydrostatic pressure through the years, will change in their structure and diameter; that this autonomic activity could be associated with an excitation of the adrenal cortex, perhaps mediated via adrenalin secretion and the anterior pituitary, leading to those evidences of sodium retention and aldosteronism which have been put forward; and that in the course of time, as arteriolar damage becomes worse, renal damage may follow in turn to produce a supplementing and finally dominant renal hy¬ pertension. This is a picture which, speculative though it is, I believe many people take as a working model. Its attraction seems to be simply that it provides a sequential analysis of hypertension, which does not seem to flow so plausibly from the other approaches. I do not know, for instance, of any satisfactory physiologic evidence that an adrenocortical overactivity could commonly give rise to a physiologic state which could be interpreted as autonomic overactivity, although, as just mentioned, one can envisage a state in which autonomic overactivity could give rise to adrenocortical activity. One can therefore, propose that the prime cause of hypertension is a sympathetic overactivity, and that the features of its later development have been elicited by this initial neurogenic excitation. SOME OBJECTIONS There are, however, still some objections to meet. The first bears almost directly on pharmacology. If you give a ganglion blocking agent to a hyper* tensive, it seems that the blood pressure only rarely falls to the same level observed for a normotensive. This provides the basis for the allotment of the excess of blood pressure over the normal into a neurogenic and non- neurogenic fraction. I am not sure, however, that this necessarily holds, be¬ cause of the difficulty in producing complete ganglion block. One must remember, for instance, that it is usually impossible to produce in an animal, with any dose of ganglion blocking agent, a blood pressure as low as that achieved by anesthesia or destruction of the spinal cord. My own guess, which I have argued elsewhere, is that the accessory ganglia, those cells located, not in the pre- and paravertebral ganglion chains, but in the rami