American Heart Association's 61st Annual High Blood Pressure Research Conference, Sept. 26-29, 2007
American Heart Association's 61st Annual High Blood Pressure Research Conference 2007
MONDAY, Oct. 8 (HealthDay News) -- The American Heart Association's 61st Annual High Blood Pressure Research Conference took place Sept. 26-29 in Tucson, Ariz., and attracted about 11,400 attendees from around the world. The conference presented research on new molecular targets and therapeutic agents for treating high blood pressure and also included studies that advance understanding of the mechanisms behind the development of high blood pressure.
"There were a lot of presentations and a lot of discussions related to new molecular targets for the treatment of high blood pressure and cardiovascular disease," said Gabriel Navar, Ph.D., of Tulane University in New Orleans, chair of the Council for High Blood Pressure Research. "Most of these targets are related to components of the renin-angiotensin system. So there was a lot of discussion about renin inhibitors, a new class of drugs that block renin directly," he said.
"There was also a lot of discussion about a new enzyme called ACE2, which is a homologue of ACE1," Navar said. "ACE2 does the opposite of ACE1. It helps break down angiotensin 2 so it can be metabolized. It does not cause vasoconstriction. So it may be possible to reduce blood pressure by increasing the activation of ACE2. Several studies showed that."
Among them was a study presented by researchers from the University of Florida in Gainesville, who identified a novel compound that doubles the activation of ACE2. They found that it reduced blood pressure and helped reverse cardiac hypertrophy and myocardial fibrosis.
The new research may lead to changes in clinical practice, Navar said. "In order to get effective control of blood pressure, especially in patients who have complex high blood pressure, researchers are suggesting it may be necessary to use a combination of renin inhibition plus either ACE inhibition or blocking of the ACE2 receptor."
Many studies addressed how genetics affect the development and progression of hypertension. This year's Novartis Award for Hypertension Research -- the council's highest honor -- went to Friedrich C. Luft, M.D., of the University of Berlin, Germany, for his work in identifying some of the chromosomes associated with high blood pressure, and for showing how high blood pressure damages the heart, kidneys and circulatory system, Navar said.
Other studies identified the hormone systems that are responsible for the kidneys' ability to excrete salt and regulate blood pressure. "One session -- 'Renal Tubular Transport and Natriuretic Factor' -- showed how new hormones such as endothelin, cyclic GMP, and nitric oxide are all importantly involved in the regulation of the ability of the kidneys to excrete salt," Navar said. "When any of these systems aren't functioning properly, the kidneys don't excrete as much salt as they should, which leads to the retention of salt and the development of high blood pressure. This helps explain why certain patients retain salt and also nicely explains why certain diuretic treatments are very important for high blood pressure."
In a surprise finding, J. Richard Jennings, Ph.D., of Emory University in Atlanta, and colleagues presented research showing that successful blood pressure treatment more than doubles the amount of brain activation needed to perform memory tasks, especially in the parietal and prefrontal cortex. "We speculate that dilated cerebral vessels related to the decrease in pressure with treatment might be less able to differentially direct cerebral blood flow to active brain areas," Jennings said.
"A positive interpretation of the results is that hypertensives are able to alter their cerebral blood flow so that their cognitive function remains largely intact," Jennings added. "Our finding suggests that this compensation is successfully maintained with successful blood pressure treatment with different medications. Patients' cognitive function was maintained with treatment -- an observation that wasn't the focus of the current presentation. Less positively, one can be concerned about whether this compensation has some cost in terms of fatigue or some types of cognitive function."
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