Serotonin enhances (amplifies) the vasoconstrictor effect of norepinephrine not only on isolated large blood vessels and isolated perfused vascular beds but also in vivo. This amplification can be observed with endogenous serotonin released from aggregating platelets and with endogenous norepinephrine released from the adrenergic nerves in the blood vessel wall. It is due to an interaction between S2-serotonergic and alpha 1-adrenergic mechanisms. Combined S2-serotonergic and alpha 1-adrenergic antagonism is more effective than either one alone against contractions evoked with the combination of serotonin and an alpha 1-adrenergic agonist. In spontaneously hypertensive rats, S2-serotonergic antagonism alone does not reduce blood pressure but combined S2-serotonergic and alpha 1-adrenergic blockade lowers blood pressure more than alpha 1-adrenergic blockade alone. This suggests that the interaction between S2-serotonergic and alpha 1-adrenergic vasoconstrictor responses may play a role in the maintenance of high blood pressure.
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Nephrol Nurs J
January 2025
Professor of Pharmacy Practice, Clinical Pharmacotherapy Specialist, Nephrology & Dialysis, Arnold &Marie Schwartz College of Pharmacy and Health Sciences, Long Island University, Brooklyn, NY.
Intradialytic hypotension (IDH) is a common occurrence in hemodialysis. IDH occurs when there is a drop in blood pressure along with hypotensive symptoms. There are various causes of IDH, and it is important to consider proper management of this condition.
View Article and Find Full Text PDFClin Auton Res
January 2025
Department of Health and Kinesiology, Purdue University, West Lafayette, Indiana, USA.
Purpose: Resting beat-to-beat blood pressure variability is a strong predictor of cardiovascular events and mortality. However, its underlying mechanisms remain incompletely understood. Given that the sympathetic nervous system plays a pivotal role in cardiovascular regulation, we hypothesized that alpha-1 adrenergic receptors (the main sympathetic receptor controlling peripheral vasoconstriction) may contribute to resting beat-to-beat blood pressure variability.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Department of Pharmacology, Physiology and Neurobiology, University of Cincinnati College of Medicine, Cincinnati, OH.
Lower body negative pressure (LBNP) has been used for decades in humans to model arterial baroreceptor unloading and represents a powerful tool for evaluating cardiovascular responses to orthostatic challenge. However, LBNP studies in animals have been limited to conditions of anesthesia or sedation, where cardiovascular reflexes are altered. Given the consequent uncertainties, the usefulness of LBNP studies in these preclinical models has been severely hampered.
View Article and Find Full Text PDFNat Neurosci
January 2025
Department of Physiology, Seoul National University College of Medicine, Seoul, Korea.
The cerebellum is activated by noxious stimuli and pathological pain but its role in noxious information processing remains unknown. Here, we show that in mice, cutaneous noxious electrical stimuli induced noradrenaline (NA) release from locus coeruleus (LC) terminals in the cerebellar cortex. Bergmann glia (BG) accumulated these LC-NA signals by increasing intracellular calcium in an integrative manner ('flares').
View Article and Find Full Text PDFNeuropharmacology
March 2025
Department of Experimental Physiology and Pathophysiology, Medical University of Białystok, Ul. Mickiewicza 2A, 15-222, Białystok, Poland.
Although angiotensin 1-7 (Ang 1-7) and its role as a part of the "protective" axis of the renin-angiotensin system are well described in the literature, the mechanisms of its angiotensin II-like pressor and tachycardic effects following its acute central administration are not fully understood. It was the aim of the present study to examine which receptors contribute to the aforementioned cardiovascular effects. Ang 1-7 and antagonists for glutamate, GABA, vasopressin, thromboxane A (TP), α-adrenergic, and P2X purinoceptors or modulators of oxidative stress were injected into the paraventricular nucleus of the hypothalamus (PVN) of urethane-anesthetized male Wistar rats.
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