Cardiovascular effects of parathyroid hormone in conscious sheep

Jordan, LR; Dallemagne, CR; Cross, R. B.

doi:10.1113/expphysiol.1991.sp003491

Cited by 3 publications

(2 citation statements)

References 24 publications

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“…In conclusion, animal models have demonstrated potential effects of PTH on the cardiovascular system [94], and these may lead to increased rates of dizziness [95] with PTH analogues. However, whether this increased risk is manifested via the cardiovascular system is not clear, and there is certainly no current evidence to suggest an increased risk of atherosclerotic or thromboembolic cardiac disease with this group of interventions.…”

Section: Parathyroid Hormone Analoguesmentioning

confidence: 95%

“…It has long been known, initially from animal studies, that PTH has chronotropic effects via receptors in cardiac myocytes and transient dilatory effects on the peripheral vasculature, leading to an increase in heart rate and reduction in blood pressure, respectively [94]. These effects may have manifested as adverse events in the trials for the two PTH analogues that are currently used in osteoporosis clinical practice: teriparatide and abaloparatide.…”

Section: Parathyroid Hormone Analoguesmentioning

confidence: 99%

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Assessment of Cardiovascular Safety of Anti-Osteoporosis Drugs

Fuggle

Cooper

Harvey

et al. 2020

Drugs

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The incidence of osteoporosis and cardiovascular disease increases with age, and there are potentially shared mechanistic associations between the two conditions. It is therefore highly relevant to understand the cardiovascular implications of osteoporosis medications. These are presented in this narrative review. Calcium supplementation could theoretically cause atheroma formation via calcium deposition, and in one study was found to be associated with myocardial infarction, but this has not been replicated. Vitamin D supplementation has been extensively investigated for cardiac benefit, but no consistent effect has been found. Despite findings in the early 21st century that menopausal hormone therapy was associated with coronary artery disease and venous thromboembolism (VTE), this therapy is now thought to be potentially safe (from a cardiac perspective) if started within the first 10 years of the menopause. Selective estrogen receptor modulators (SERMs) are associated with increased risk of VTE and may be related to fatal strokes (a subset of total strokes). Bisphosphonates could theoretically provide protection against atheroma. However, data from randomised trials and observational studies have neither robustly supported this nor consistently demonstrated the potential association with atrial fibrillation. Denosumab does not appear to be associated with cardiovascular disease and, although parathyroid hormone analogues are associated with palpitations and dizziness, no association with a defined cardiovascular pathology has been demonstrated. Finally, romosozumab has been shown to have a possible cardiovascular signal, and therefore post-market surveillance of this therapy will be vital.

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Section: Parathyroid Hormone Analoguesmentioning

confidence: 95%

Section: Parathyroid Hormone Analoguesmentioning

confidence: 99%

Assessment of Cardiovascular Safety of Anti-Osteoporosis Drugs

Fuggle

Cooper

Harvey

et al. 2020

Drugs

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Effects of PTH(1-34) on Blood Pressure, Renal Function, and Hormones in Essential Hypertension The Altered Pattern of Reactivity May Counteract Raised Blood Pressure

Jespersen

Randløv

Abrahamsen

et al. 1997

American Journal of Hypertension

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As it has been suggested that parathyroid hormone (PTH) is implicated in the pathophysiology of essential hypertension, the effects of PTH(1-34) were assessed during infusion over 120 min in ten men with essential hypertension and in ten healthy men. Ionized calcium was kept constant by a clamping technique. Mean arterial blood pressure fell slightly in the patients (116 mm Hg, median, before, and 108 mm Hg during the infusion, P < .01), but remained unchanged in the controls (median 87 mm Hg). The pulse rate rose to a similar extent in the two groups, but cardiac output, measured by the CO2 rebreathing technique, was unchanged. The glomerular filtration rate (GFR) was slightly lower in the hypertensives than in the controls at baseline (92 v 109 mL/min, P < .02), but it increased similarly during PTH infusion in both groups (+13% v +9%, medians), as did the effective renal plasma flow (+50% v +38%). The urinary rate of sodium excretion, which was similar at baseline, increased more in the patients than in the controls (+191% v +46%, P < .05); this was mainly attributable to a reduction in the tubular reabsorption of sodium. Calculations based on lithium clearance indicated that mainly the proximal tubular reabsorption of sodium decreased during PTH infusion. Baseline plasma PTH(1-84) was higher in the patients than in the controls (20.5 ng/L v 16.5 ng/L, P < .05). The baseline plasma values of renin, aldosterone, atrial natriuretic peptide, endothelin, and noradrenaline were similar in the two groups. During infusion of PTH, renin increased less in the patients than in the controls (P < .02), and aldosterone increased only in the controls (P < .01). The other hormonal values remained unchanged. In conclusion, the patients with essential hypertension had increased baseline PTH values, but nevertheless PTH had more marked vasodilative and natriuretic effects than in the controls. PTH thus seems to counteract rather than aggravate elevation of blood pressure in these patients.

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Signaling Pathway and Chronotropic Action of Parathyroid Hormone in Isolated Perfused Rat Heart

Shimoyama

Oginö

Furuse

et al. 2001

Journal of Cardiovascular Pharmacology

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Parathyroid hormone (PTH) activates both adenylyl cyclase and phospholipase C via the PTH-1 receptor. We previously reported that PTH increased heart rate and that this effect was mediated via the pacemaker current (I f ). However, it has been reported that PTH exerts its chronotropic effect via an interaction with adrenergic receptors or via L-type calcium channels. Thus, the objective of the study was to elucidate the exact mechanism of the chronotropic effect of PTH. We tested whether its chronotropic effects could be abolished by inhibitors of the following systems in isolated perfused rat hearts: alpha-adrenergic (prazosin); beta-adrenergic (propranolol); angiotensin II (CV11974); endothelin-1 (TAK044); calcium channel (verapamil); adenylyl cyclase (miconazole); phospholipase C (U73122) or I f (CsCl). In addition, we measured the cyclic adenosine monophosphate level of the heart after PTH administration. Whereas prazosin, propranolol, CV11974, TAK044, verapamil, and U73122 did not inhibit the chronotropic effect of PTH, CsCl or miconazole suppressed it significantly. PTH increased the cyclic adenosine monophosphate level of the atrium but not the left ventricle. These results indicate that the chronotropic actions of PTH are mediated via selective activation of adenylyl cyclase to increase the I f current.

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Cardiovascular effects of parathyroid hormone in conscious sheep

Cited by 3 publications

References 24 publications

Assessment of Cardiovascular Safety of Anti-Osteoporosis Drugs

Assessment of Cardiovascular Safety of Anti-Osteoporosis Drugs

Effects of PTH(1-34) on Blood Pressure, Renal Function, and Hormones in Essential Hypertension The Altered Pattern of Reactivity May Counteract Raised Blood Pressure

Signaling Pathway and Chronotropic Action of Parathyroid Hormone in Isolated Perfused Rat Heart

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