Biomedical subjects

S B Plant

Publications and source records attributed to S B Plant.

4 recordsLinked to original sources

PubMed1984

cAMP response of vascular smooth muscle cells to bovine parathyroid hormone.

Parathyroid hormone (PTH) is a vasodilator of vascular smooth muscle tissue. It has been shown to produce this vasodilation in normotensive and hypertensive laboratory rats. The effect is log dose dependent, maximal at 1 min and persists for 3-5 min. The cellular mechanisms involved in PTH-mediated vasodilation are unknown. In this study, we sought to determine the cellular changes of cAMP after administration of bovine (b)PTH (1-34). cAMP content of vascular smooth muscle cells was measured at 30 s, 1, 3, and 5 min after incubation with synthetic bPTH (1-34). Tissue cAMP content was decreased by 55% at 1 min (4.1 +/- 0.5 pmol/mg protein at time 0 vs. 1.9 +/- 0.2 pmol/mg protein at 1 min, P less than 0.001). After 5 min, cAMP levels returned to base-line values and increased over the next 5-10 min to levels above base line (P less than 0.01). In conclusion, our data suggest that the initial response of vascular smooth muscle cells to short-term incubation with bPTH (1-34) is an acute decrease in cAMP content.

Animals↗

PubMed1982

Gentamicin does not chelate calcium.

The influence of increasing gentamicin concentrations on ionized calcium concentration was determined in pH-controlled, phosphate-buffered saline and normal human serum with an ion-specific calcium electrode. No evidence of calcium chelation was found.

Calcium↗

PubMed1982

Ionized calcium and the in vivo response of normal and hyperplastic parathyroid glands to beta-adrenergic agents.

We compared ionized serum calcium and parathyroid hormone (PTH) responses to the beta-adrenergic agents, isoproterenol and propranolol, in 14 patients with hyperparathyroidism following renal transplantation and 8 normal volunteers. Following isoproterenol, PTH rose in normal subjects concurrent with a significant (p less than 0.01) fall in ionized but not total, calcium. In the hyperparathyroid patients the PTH concentration decreased (p less than 0.001) coincident with a significant (p less than 0.01) increase in ionized, but not total, calcium. Changes in both PTH (p less than 0.05) and ionized calcium (p less than 0.05) were significantly different in hyperparathyroid patients compared to normal subjects. Propranolol did not affect PTH, ionized or total calcium in either group. We conclude that beta-adrenergic stimulation of PTH secretion may be mediated, in part, by antecedent changes in ionized calcium and not solely a direct effect of the agonist. Concurrent assessment of changes in ionized calcium is necessary for proper interpretation of investigations involving the sympathetic nervous system's regulation of PTH secretion.

Adult↗

PubMed1981

Parathyroid hormone: a determinant of posttransplant blood pressure regulation.

Persistent hyperparathyroidism and its attendant hypercalcemia have been implicates as possible etiologic factors in posttransplant hypertension. To better define the role of parathyroid hormone (PTH) and calcium in posttransplant blood pressure homeostasis, we measured the acute response of blood pressure, ionized calcium (Ca++), plasma renin activity (PRA), and parathyroid hormone (PTH) to a 4-hr infusion of calcium (15 mg/kg) and an isoproterenol injection (0.15 mg SC) in seven normal subjects and 13 renal transplant (Tx) recipients with stable graft function and persistent hyperparathyroidism. Transient hypercalcemia produced a significant (p less than 0.01) increase in the systolic blood pressure (delta SBP) and suppression of PTH (p less than 0.001) in the posttransplant subjects. There was a significant (p less than 0.02) inverse correlation between changes (delta) in PTH and delta SBP in these subjects. There was no correlation between the delta SBP and either the change in Ca++ (delta Ca++) or the change in PRA (delta PRA) observed in the Tx recipients administered calcium. Following isoproterenol administration, SBP increased (p less than 0.01), PTH fell (p less than 0.05) and Ca++ was only minimally increased in the Tx recipients. A virtually identical, significant (p less than 0.05) inverse correlation existed between the delta PTH and delta SBP observed in the transplant subjects. Greater suppression of PTH was associated with a larger increase in systolic blood pressure. Transient hypercalcemia of comparable degree in normal subjects caused an insignificant increase in their blood pressure. The fact that PTH suppression in the normals was substantially (0.01) less (delta PTH -13 microliter/Eq/ml versus -65 microliter/Eq/ml in the transplant group) with a similar increase in serum calcium suggests that the blood pressure response to transient hypercalcemia is more dependent on PTH suppression than the level of ionized calcium. Plasma renin activity was unchanged during the blood pressure fluctuations induced by either the calcium or the isoproterenol administration to the normal subjects. Under the conditions of this study, endogenous parathyroid hormone has the characteristics of a vasodepressor hormone and may have a role in blood pressure regulation in transplant recipients with hyperparathyroidism. Since the vasodepressor effect can be dissociated from delta Ca+ and delta PRA, such a conclusion seems warranted. The implications of these findings for all subjects with renal disease requires further investigation.

Blood Pressure↗