The Role of Sex Steroids in Angiogenesis

Author(s):  
Yuen Ting Lam ◽  
Laura Lecce ◽  
Christina A. Bursill ◽  
Martin K. C. Ng
Keyword(s):  
2021 ◽  
Author(s):  
L Ratten ◽  
E Plummer ◽  
C Bradshaw ◽  
C Fairley ◽  
S Garland ◽  
...  

Author(s):  
Anatoly E Martynyuk ◽  
Ling-Sha Ju ◽  
Timothy E Morey

Abstract Most surgical procedures require general anesthesia, which is a reversible deep sedation state lacking all perception. The induction of this state is possible because of complex molecular and neuronal network actions of general anesthetics (GAs) and other pharmacological agents. Laboratory and clinical studies indicate that the effects of GAs may not be completely reversible upon anesthesia withdrawal. The long-term neurocognitive effects of GAs, especially when administered at the extremes of ages, are an increasingly recognized health concern and the subject of extensive laboratory and clinical research. Initial studies in rodents suggest that the adverse effects of GAs, whose actions involve enhancement of GABA type A receptor activity (GABAergic GAs), can also extend to future unexposed offspring. Importantly, experimental findings show that GABAergic GAs may induce heritable effects when administered from the early postnatal period to at least young adulthood, covering nearly all age groups that may have children after exposure to anesthesia. More studies are needed to understand when and how the clinical use of GAs in a large and growing population of patients can result in lower resilience to diseases in the even larger population of their unexposed offspring. This minireview is focused on the authors’ published results and data in the literature supporting the notion that GABAergic GAs, in particular sevoflurane, may upregulate systemic levels of stress and sex steroids and alter expressions of genes that are essential for the functioning of these steroid systems. The authors hypothesize that stress and sex steroids are involved in the mediation of sex-specific heritable effects of sevoflurane.


2018 ◽  
Vol 9 (1) ◽  
pp. 150 ◽  
Author(s):  
Gustavo Pradilla ◽  
JackW Barrow ◽  
Nefize Turan ◽  
Pasang Wangmo ◽  
AnilK Roy

Author(s):  
ALISON M. DUNCAN ◽  
WILLIAM R. PHIPPS ◽  
MINDY S. KURZER
Keyword(s):  

1999 ◽  
Vol 276 (6) ◽  
pp. H2063-H2068 ◽  
Author(s):  
Michelle Grewal ◽  
Janis Cuevas ◽  
Gautam Chaudhuri ◽  
Lauren Nathan

It has been demonstrated in reflex-intact animals that the sensitivity to calcitonin gene-related peptide (CGRP) is increased during pregnancy and that this action is mediated by sex steroids but not by nitric oxide (NO). We assessed the effects of CGRP in the following groups of anesthetized ganglion-blocked rats: 1) pregnant, 2) ovariectomized, and 3) ovariectomized and treated with estradiol and progesterone. Changes in mean arterial pressure (MAP) were assessed after the administration of varying doses of CGRP. Decreases in MAP after CGRP administration were significantly greater in pregnant rats and ovariectomized rats administered sex steroids than in ovariectomized controls. The CGRP antagonist CGRP8–37 produced a pressor response of similar magnitude in both pregnant and ovariectomized rats. We also assessed the effects of CGRP and the modulating role of NO in the isolated uterine vascular bed preparation. CGRP reduced perfusion pressure to a greater degree in ovariectomized animals treated with sex steroids than in ovariectomized animals. This response was attenuated by pretreatment with an NO synthesis inhibitor. CGRP8–37 produced a similar increase in perfusion pressure in both groups. We conclude that 1) the increased vascular sensitivity observed during pregnancy or after treatment with sex steroids is in part mediated by NO, and 2) CGRP8–37 has a vasoconstrictor action of its own.


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