EMBARGOED PER JCI UNTIL APRIL 17,1996                                                        



                                                 CONTACT: Marguerite Beck

	U.VA. RESEARCHERS FIND KEY TO A CAUSE OF HYPERTENSION

	CHARLOTTESVILLE, VA., April 16 -- Scientists at the University of 
Virginia have unlocked a door into one cause of high blood pressure and 
related cardiovascular disease, according to a study published in the April 
17 issue of The Journal of Clinical Investigation.
	Drs. Helmy M. Siragy and Robert M. Carey have identified the function 
of a recently discovered cell receptor of angiotensin II, a powerful hormone 
that regulates blood pressure and salt and fluid retention. Although the 
receptor, AT2, was identified a few years ago, its role remained unknown.
	"Identifying the function of AT2 receptors may help researchers gain 
a greater understanding of cardiovascular and kidney disease and lead to the 
development of better treatments," Siragy said. "In the majority of patients 
with hypertension, doctors don't know the cause, sot they have to try 
different drugs to control the pressure, often with unwanted side effects."
	Prior to this study, researchers believed that angiotensin II acted 
through a single receptor, AT1. Excess activity of the AT1 receptor has been 
implicated in the development of hypertension, congestive heart failure and 
diabetic kidney disease.
	Using kidney microdialysis, a technique developed by Siragy and 
Carey that utilizes a hair thin catheter inserted in the kidney, the 
researchers conducted studies to monitor the activity of AT2 receptors in 
rats. By varying the salt intake and pharmacologically blocking or 
stimulating the receptors, they discovered that AT2 receptors play an 
unexpected role in the activity of the hormone. 
	While AT1 receptors constrict blood vessels to elevate blood 
pressure, AT2 receptors relax blood vessels to lower blood pressure. The two 
angiotensin receptors act in opposition to one another to balance the 
hormone's activity. The study showed that AT1 receptors stimulate 
prostaglandin production, while AT2 receptors limit that effect.
	In addition, researchers found that AT2 receptor stimulation results 
in increased renal production of a vasodilating substance called cylic GMP. 	
           Siragy and Carey suspect that some people may lack AT2 receptors 
or have reduced AT2 activity, which theoretically could lead to the 
development of high blood pressure. Developing drugs that could mimic AT2 or 
stimulate its activity could help doctors treat a specific cause of the 
disease, not just the symptoms.

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						April 16, 1996