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R F Spark

Publications and source records attributed to R F Spark.

At least 37 records · Page 2Linked to original sources
PubMed1969

Activation of aldosterone secretion in primary aldosteronism.

Angiotensin infusion evokes marked increases in aldosterone secretion in primary aldosteronism and little change in secondary aldosteronism. The low plasma renin activity of primary aldosteronism and the elevated plasma renin activity of secondary aldosteronism are thought to account for this differential response. The effect of angiotensin on aldosterone and 18-hydroxycorticosterone secretion was studied during adrenal vein catheterization in seven patients with primary aldosteronism (whose plasma renin activity had been elevated following spironolactone therapy), one hypertensive patient with normal plasma renin activity and normal aldosterone secretion, two patients with secondary aldosteronism who had elevated plasma renin activity, and one anephric patient whose plasma renin activity was 0. Adrenal venous aldosterone and 18-hydroxycorticosterone were measured before and after a ten min sub-pressor angiotensin infusion. The cells of the aldosterone-producing adenoma (APA) respond to small increases in plasma angiotensin with large increases in secretion of aldosterone and 18-hydroxycorticosterone. The dose of angiotensin capable of evoking this response from the aldosterone-producing adenoma produces little or no change in the secretion of the steroids from nontumorous glands. The augmentation of aldosterone secretion, induced by angiotensin, in primary aldosteronism is due solely to increased secretion by the adenoma and not by the contralateral zona glomerulosa. The increased sensitivity of the aldosterone-producing adenoma is characteristic of the tumor. This response is independent of fluctuations in endogenous plasma renin activity. This sensitivity is not blunted by high plasma renin activity, nor is it a function of tumor mass for the effect is observed in aldosterone-producing adenomas regardless of size. ACTH injection after angiotensin infusion resulted in a marked increase in aldosterone concentration in the effluent from the nontumorous adrenal, but was not capable of producing further increases in aldosterone concentration in the effluent from the APA. In view of this exquisite sensitivity to infused angiotensin, it may be that the small variations in endogenous plasma renin activity that have been observed in primary aldosteronism may be capable of evoking large changes in aldosterone secretion in patients with aldosterone-producing adenomas.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Intrinsa fails to impress FDA advisory panel.

Female sexual dysfunction (FSD) as a discipline of medicine is not fully recognized by many authorities. Definitions are controversial and data are lacking, yet the public clamors for treatment. The lay press has capitalized on this provocative women's issue, seizing on the public's insatiable desire for new, potentially 'sexy' therapeutic options in this area. Thus, the time was ripe for a potential FSD drug. The sexual medicine community watched with interest as the Food and Drug Administration (FDA) considered the Proctor & Gamble new drug application for Intrinsa (a testosterone patch for hypoactive sexual desire disorder for women who had undergone surgical castration via bilateral oophorectomy). In spite of quality scientific data, Intrinsa was not approved. With this issue of IJIR, a new column, entitled, 'perspective' is provided to the readership. Perspective is an invited opinion or viewpoint that aims to advise and update the medical community on a pertinent or current topic in sexual medicine. Dr Richard Spark, a noted endocrinologist, presents the first of three invited 'perspectives' on Intrinsa and the FDA decision. Dr Spark has authored several manuscripts on the topic of FSD.

Administration, Cutaneous↗