A developmental genetic mechanism involving angiotensin in spontaneously hypertensive rats.
1. Certain genes drive the blood pressure of young spontaneously hypertensive rats (SHR) to stable hypertensive levels in adulthood. 2. Relatively brief blockade of the renin-angiotensin system in young SHR can reset the track of SHR pressure to a lower level for the life of the animal. This effect appears to be a characteristic of the SHR strain. 3. It is proposed that the expression of a particular SHR hypertensive gene depends on angiotensin and is limited to young animals. This hypothesis explains some of the phenotypic abnormalities observed in young SHR and the decremental long-term blood pressure effects following ACE inhibitor treatment. 4. The identity of the gene is unclear, but information from biochemical, physiological and pharmacological studies may direct attention to distinct candidate genes within specific chromosomal regions of interest. 5. Understanding these genetic mechanisms may have important implications for future preventive strategies.
Harrap
S B
SB
Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia.
D000375:Aging / Q000502:physiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D015870:Gene Expression / Q000187:drug effects; D006973:Hypertension / Q000235:genetics*; D051381:Rats; D011918:Rats, Inbred SHR; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors