Effect of vasopressin-induced chronic hyponatremia on the regulation of the middle cerebral artery of the rat

Aleksandrowicz, Marta; Koźniewska, Ewa

doi:10.1007/s00424-018-2141-0

Cited by 4 publications

(3 citation statements)

References 39 publications

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“…As the s.c. administration of LIT01-196 increased aqueous diuresis, we investigated whether LIT01-196 could be used to reverse the antidiuretic effect of AVP in vivo. AVP infusion has been shown to induce hyponatremia efficiently 43 , 44 , and did not induce excessive mortality 43 . We therefore chose to use AVP to induce hyponatremia in rodents, to obtain an SIAD model resembling the disease observed in humans.…”

Section: Discussionmentioning

confidence: 99%

A metabolically stable apelin-17 analog decreases AVP-induced antidiuresis and improves hyponatremia

et al. 2021

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Apelin and arginine-vasopressin (AVP) are conversely regulated by osmotic stimuli. We therefore hypothesized that activating the apelin receptor (apelin-R) with LIT01-196, a metabolically stable apelin-17 analog, may be beneficial for treating the Syndrome of Inappropriate Antidiuresis, in which AVP hypersecretion leads to hyponatremia. We show that LIT01-196, which behaves as a potent full agonist for the apelin-R, has an in vivo half-life of 156 minutes in the bloodstream after subcutaneous administration in control rats. In collecting ducts, LIT01-196 decreases dDAVP-induced cAMP production and apical cell surface expression of phosphorylated aquaporin 2 via AVP type 2 receptors, leading to an increase in aqueous diuresis. In a rat experimental model of AVP-induced hyponatremia, LIT01-196 subcutaneously administered blocks the antidiuretic effect of AVP and the AVP-induced increase in urinary osmolality and induces a progressive improvement of hyponatremia. Our data suggest that apelin-R activation constitutes an original approach for hyponatremia treatment.

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Section: Discussionmentioning

confidence: 99%

A metabolically stable apelin-17 analog decreases AVP-induced antidiuresis and improves hyponatremia

et al. 2021

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“…Differences between MCAs and PAs in our study are also noticeable in the reactivity of these vessels to an increase in extravascular K + concentration. Twenty mmol/L K + solution, used to verify the viability of isolated MCAs in our study, is a routine test used for this purpose 25‐28 . It occurred, however, that PAs are more responsive than MCAs to the increase in extravascular K + concentration which is demonstrated by the dilation of PAs to 10 mmol/L K + to a similar extent as the dilation of the MCAs to 20 mmol/L K + solution (88% vs. 85% of the basal diameter).…”

Section: Discussionmentioning

confidence: 77%

Compromised regulation of the rat brain parenchymal arterioles in vasopressin‐associated acute hyponatremia

Aleksandrowicz

Koźniewska

2020

Microcirculation

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Objective In this study, we examined the effect of acute hyponatremia associated with vasopressin (AVP) on the responses of the isolated rat's MCAs and PAs to acidosis, nitric oxide donor (SNAP) and to endothelium‐dependent vasodilator ATP. Methods The studies were performed on isolated, perfused and pressurized MCAs and PAs in control conditions and during AVP‐associated hyponatremia. Hyponatremia was induced in vitro by lowering Na+ concentration from 144 to 121 mmol/L in intra‐ and extravascular fluid in the presence of AVP. Results Parenchymal arterioles showed greater response to an increase in H+ and K+ ions concentration and to ATP in comparison with MCAs in control normonatremic conditions. Both PAs and MCAs constricted in response to acute hyponatremia associated with AVP. Interestingly, disordered regulation of vascular tone was observed in PAs but not in MCAs. The abnormalities in the regulation comprised a significant reduction of PA response to acidosis and the absence of the response to the administration of SNAP or ATP. Conclusions Arginine vasopressin‐associated hyponatremia leads to constriction and dysregulation of PAs which may impair neurovascular coupling.

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“…In the cerebral circulation, vasopressin can cause either increase of the blood flow through an action mediated by V2Rs [85] or restriction of the flow, presumably through stimulation of V1Rs. Interestingly, it appears that the vasoconstrictory action of vasopressin in the cerebral circulation may predominate in hyponatremia, which is an unavoidable attribute of SIADH [168,169]. The traumatic brain injury which is associated with hypoxia causes significant increase of V1aR in the frontoparietal cortex [104].…”

Section: Function Of Vasopressin System In Cardiovascular Diseasesmentioning

confidence: 99%

Vasopressin: a possible link between hypoxia and hypertension

Szczepañska‐Sadowska

Żera

2022

Exploration of Medicine

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Cardiovascular and respiratory diseases are frequently associated with transient and prolonged hypoxia, whereas hypoxia exerts pro-hypertensive effects, through stimulation of the sympathetic system and release of pressor endocrine factors. This review is focused on the role of arginine vasopressin (AVP) in dysregulation of the cardiovascular system during hypoxia associated with cardiovascular disorders. AVP is synthesized mainly in the neuroendocrine neurons of the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON), which send axons to the posterior pituitary and various regions of the central nervous system (CNS). Vasopressinergic neurons are innervated by multiple neuronal projections releasing several neurotransmitters and other regulatory molecules. AVP interacts with V1a, V1b and V2 receptors that are present in the brain and peripheral organs, including the heart, vessels, lungs, and kidneys. Release of vasopressin is intensified during hypernatremia, hypovolemia, inflammation, stress, pain, and hypoxia which frequently occur in cardiovascular patients, and blood AVP concentration is markedly elevated in cardiovascular diseases associated with hypoxemia. There is evidence that hypoxia stimulates AVP release through stimulation of chemoreceptors. It is suggested that acting in the carotid bodies, AVP may fine-tune respiratory and hemodynamic responses to hypoxia and that this effect is intensified in hypertension. There is also evidence that during hypoxia, augmentation of pro-hypertensive effects of vasopressin may result from inappropriate interaction of this hormone with other compounds regulating the cardiovascular system (catecholamines, angiotensins, natriuretic peptides, steroids, nitric oxide). In conclusion, current literature indicates that abnormal mutual interactions between hypoxia and vasopressin may significantly contribute to pathogenesis of hypertension.

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Effect of vasopressin-induced chronic hyponatremia on the regulation of the middle cerebral artery of the rat

Cited by 4 publications

References 39 publications

A metabolically stable apelin-17 analog decreases AVP-induced antidiuresis and improves hyponatremia

A metabolically stable apelin-17 analog decreases AVP-induced antidiuresis and improves hyponatremia

Compromised regulation of the rat brain parenchymal arterioles in vasopressin‐associated acute hyponatremia

Vasopressin: a possible link between hypoxia and hypertension

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