Emory Report

January 12, 1998

 Volume 50, No. 16

Bernstein receives prestigious
MERIT award from NIH

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health has granted Kenneth Bernstein, professor of pathology and laboratory medicine, a MERIT award in recognition of his "consistent and excellent contributions to scientific knowledge."

MERIT (Method to Extend Research in Time) awards extend the normal time period for a research grant, providing outstanding investigators with the opportunity for long-term support that will enhance their continued scientific creativity and lessen the administrative burdens of preparing and submitting grant applications. The $2 million MERIT award is an eight-year grant extending Bernstein's original NIH grant, awarded in 1988 when he first joined Emory. He also is an investigator under Emory's O'Brien Kidney Center grant and principal investigator for three other NIH grants.

During the past 10 years Bernstein and his colleagues have been responsible for a number of key scientific discoveries that have transformed the way scientists view the renin-angiotensin system and its effects on cardiovascular function. In 1989 they became one of the first laboratories in the world to isolate and clone the gene for the angiotensin converting enzyme (ACE), which controls the production of angiotensin II-the link between the kidneys and blood pressure control.

When blood pressure drops, the kidney attempts to counterbalance the drop by releasing the enzyme renin. Renin in turn catalyzes the production of angiotensin, a hormone circulating in the blood. The ACE enzyme converts the inactive form of angiotensin-antiotensin I-to angiotensin II, which is a powerful constricter of blood vessels.

Angiotensin II raises blood pressure and decreases fluid loss by the kidney. For example, angiotensin II stimulates the adrenal cortex to secrete aldosterone, which regulates the body's electrolyte and water balance by promoting the retention of sodium (and therefore of water) and the excretion of potassium. The retention of water induces an increase in plasma volume and thus an increase in blood pressure.

"Everybody would accept the fact that while blood pressure is very complex and multifactorial," Bernstein said, "in the middle is angiotensin II with its many effects on smooth muscle, the heart, the kidney, the adrenal, the brain and the gut, all of which maintain blood pressure. By understanding and cloning this receptor, we have given people an immense, powerful tool to study the regulation of blood pressure and to understand this multisystem process that maintains our blood."

One of the most interesting aspects of ACE biology is the two different manifestations, or isozymes, of the enzyme. The terms for these two different isozymes-somatic ACE and testis ACE-were first coined by Bernstein's group. Somatic ACE, found in the lungs, the kidneys and in blood vessels throughout the body, is the form commonly associated with control of blood pressure, but the other form-testis ACE-is made exclusively by developing male sperm cells.

Bernstein's study of testis ACE has focused on two critical dilemmas: How is this unique form of ACE made in such a restricted, tissue-specific fashion? And is there any real physiological role of testis ACE in male reproductive biology?

"These are very fundamental questions that go to the very basis of what makes one cell different from another cell," Bernstein said. "By understanding the function of testis ACE, we get a real insight into the basic makeup of what we are, which is a creature of many different tissues, each of which is responsible for a functionality."

-Lorri Preston

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