AMUIRHEAD E. E.

ANDERSON E.

BRAUN-MEN Ez, E

BRAUN-MENE NDEZ

BRAUN-MENENDEZ E.

GOLDBLATT H.

KOLFF W. J.

LEHR D.

MASSON G.

OGDEN F..

PAGE E. W.

PAGE I. H.

SALGADO E.

VENTURA J.

Most of the methods used for the production of experimental renal hypertension involve a reduction in the amount of functional renal tissue. According to the renotrophin hypothesis, the blood pressure of animals with experimental hypertension should be reduced or normalized if the rate of production of renotrophin is reduced (hypophysectomy, thyroidectomy, low protein diet) or if the functional renal mass is increased (kidney transplant, parabiosis). Conversely, the blood pressure should rise to higher levels or hypertension develop if the rate of production of renotrophin is increased (thyroid hormones, somatotrophin, testosterone, thyrotrophin, gonadotrophin in males, protein-rich diets) or if the functional renal mass is further reduced (sensitizing actions of unilateral nephrectomy, etc.). Experimental evidence to be presented conforms with the renotrophin hypothesis and its 4 corollaries.</jats:p

E. BRAUN-MENÉNDEZ

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Circulation

Evidence for Renotrophin as a Causal Factor in Renal Hypertension

Evidence for Renotrophin as a Causal Factor in Renal Hypertension

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