Antihypertensive Renal Effects

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In response to some stimuli (e.g., fright), catecholamines are secreted, causing renin to be released from the kidney juxtaglomerular apparatus. Renin stimulates the production of angiotensin II (Figure 15-7), and blood pressure elevation ensues from enhanced aldosterone production, Na+ reabsorption, and constrictive effects on the vasculature. In response to the increased pressure, there is increased blood flow in the renal medulla, resulting in the release of PGA2 or PGE2 (see Chapter 15).

-/3-Oxidation COOH

~-fi Oxidation

-15-Hydroxyprostaglandin NA M "*-PG Reductase Dehydrogenase the release of substance P, or whether PGE merely changes the properties of the nociceptor membrane, which results in increased firing. The elevated cyclic AMP, if involved, somehow produces pain, which, if persistent, results in a stress response via the hypothalamus (CRH) to release ACTH and then Cortisol from the adrenal gland. In addition to ACTH, (i-lipotropin is formed in equivalent amounts, which is processed to enkephalin via /^-endorphin, and enkephalin binds to a cell membrane receptor, which may compete with the PGE receptor in some way or produce a second messenger opposing the action of cyclic AMP.

Elevated levels of circulating Cortisol may produce a polypeptide, called "lipocortin" or annexin I (—40,000 Da), in the same cells that originally produced the elevated PGEs. This polypeptide is an inhibitor of phospholipase A2 and thus quenches the production of PGEs leading to pain in the first place. This is expected to be a slower process than the analgesia produced by enkephalin. In addition, there are direct nervous connections between the hypothalamus and the adrenal medulla, which lead to the release of epinephrine and enkephalins in large amounts. The function of medulla enkephalin is presently unknown; however, it may have a positive action in counteracting pain and

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