Parathyroid hormone's cardiovascular effects were assessed in a model of experimental hypertension with known abnormalities of calcium metabolism. Mean arterial pressure (MAP) changes and serum ionized calcium responses were measured in the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto (WKY), following injections of synthetic human PTH 1-34. Six 22-wk-old SHR and six WKY were given intra-arterial serial injections (0.1-100 μg/kg) of hPTH 1-34. Both the SHR (P<0.001) and WKY (P<0.001) demonstrated log dose-dependent hypotensive responses that wee maximal at 1 min, with recovery occurring between 15 and 30 min. The slopes, however, of the dose-response curves differed (P<0.01). The SHR experienced a greater maximal ΔMAP[-93.7 ± 2.4 (SHR) vs. -71.2 ± 1.6 mmHg (WKY), P<0.01]. Furthermore, the duration of the hypotensive action of hPTH 1-34 was significantly longer (P<0.001) in the SHR. Even when corrected for base-line MAP the SHR demonstrated a significant (P = 0.025) enhancement of this vasodilator response at doses of 5 μg/kg and greater at time intervals between 3 and 9 min afer injection. A transient decrease [2.25 ± 0.10 (pre) vs. 2.17 ± 0.11 meq/liter (1 min post), P<0.001] in serum ionized calcium occurred at 1 min. We conclude that hPTH 1-34 is a potent vasoactive peptide in both the normotensive WKY and the SHR. The greater maximal hypotensive response to hPTH 1-34 and the prolongation of this cardiovascular effect in the SHR may be an additional manifestation of this experimental animal's acknowledged abnormalities of cellular membrane calcium and phospholipid metabolism.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - Jan 1 1984|
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