PMID- 8732997
OWN - NLM
STAT- MEDLINE
DCOM- 19961127
LR  - 20190821
IS  - 0039-128X (Print)
IS  - 0039-128X (Linking)
VI  - 61
IP  - 4
DP  - 1996 Apr
TI  - Mineralocorticoids, salt and high blood pressure.
PG  - 184-8
AB  - Essential hypertensive patients often respond to treatments mitigating 
      mineralocorticoid action, even though circulating levels of these steroids are 
      within normal ranges. In addition to the kidney, mineralocorticoid or Type I 
      receptors are found in the brain and vascular smooth muscle where they mediate 
      effects associated with several forms of experimental hypertension. Studies in 
      which discrete anatomic or functional areas of the brain have been ablated 
      demonstrate that the periventricular areas of the hypothalamus and the central 
      sympathetic and baroreceptor systems are crucial for the development of 
      hypertension in the renoprival, DOCA salt, and Dahl salt-sensitive rat. 
      Intracerebroventricular (i.c.v.) infusion of aldosterone in both rats and dogs at 
      doses that do not raise serum levels above normal produce hypertension. The 
      hypertension produced by systemic mineralocorticoid excess, adrenal regeneration, 
      and i.c.v. or oral administration of glycyrrhetinic acid or carbenoxolone in 
      genetically normotensive rats and by dietary salt in the Dahl salt-sensitive rat 
      is inhibited by the i.c.v. infusion of a mineralocorticoid receptor antagonist or 
      a Na+ channel-selective amiloride analog. Recent data demonstrate the 
      extraadrenal synthesis of steroids in aortic endothelial cells, smooth muscle 
      cells and the brain. The role of the extraadrenal synthesis of steroids raises 
      new avenues for research into the causes of hypertension.
FAU - Gomez-Sanchez, E P
AU  - Gomez-Sanchez EP
AD  - Department of Internal Medicine, University of Missouri-Columbia, USA.
FAU - Zhou, M
AU  - Zhou M
FAU - Gomez-Sanchez, C E
AU  - Gomez-Sanchez CE
LA  - eng
GR  - HL27255/HL/NHLBI NIH HHS/United States
GR  - HL27737/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Steroids
JT  - Steroids
JID - 0404536
RN  - 0 (Adrenal Cortex Hormones)
RN  - 0 (Mineralocorticoids)
RN  - 0 (Salts)
RN  - EC 1.14.15.4 (Steroid 11-beta-Hydroxylase)
SB  - IM
MH  - Adrenal Cortex Hormones/biosynthesis
MH  - Adrenal Glands/*physiology
MH  - Animals
MH  - Blood Pressure/*drug effects/genetics
MH  - Dogs
MH  - Humans
MH  - Hypertension/*drug therapy/genetics
MH  - Mineralocorticoids/metabolism/*pharmacology
MH  - Mutation
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Regeneration/*drug effects
MH  - Salts/metabolism/pharmacology
MH  - Steroid 11-beta-Hydroxylase/genetics
RF  - 51
EDAT- 1996/04/01 00:00
MHDA- 1996/04/01 00:01
CRDT- 1996/04/01 00:00
PHST- 1996/04/01 00:00 [pubmed]
PHST- 1996/04/01 00:01 [medline]
PHST- 1996/04/01 00:00 [entrez]
AID - 0039-128X(96)00010-4 [pii]
AID - 10.1016/0039-128x(96)00010-4 [doi]
PST - ppublish
SO  - Steroids. 1996 Apr;61(4):184-8. doi: 10.1016/0039-128x(96)00010-4.