scholarly journals Complementary Role of Oxytocin and Vasopressin in Cardiovascular Regulation

2021 ◽  
Vol 22 (21) ◽  
pp. 11465
Author(s):  
Ewa Szczepanska-Sadowska ◽  
Agnieszka Wsol ◽  
Agnieszka Cudnoch-Jedrzejewska ◽  
Tymoteusz Żera
Keyword(s):  
Brain Cortex ◽  
Adrenal Glands ◽  
Cardiovascular Regulation ◽  
Peripheral Organs ◽  
Carotid Bodies ◽  
Complementary Role ◽  
Vasopressin Secretion ◽  
Volume Blood ◽  
The Brain

The neurons secreting oxytocin (OXY) and vasopressin (AVP) are located mainly in the supraoptic, paraventricular, and suprachiasmatic nucleus of the brain. Oxytocinergic and vasopressinergic projections reach several regions of the brain and the spinal cord. Both peptides are released from axons, soma, and dendrites and modulate the excitability of other neuroregulatory pathways. The synthesis and action of OXY and AVP in the peripheral organs (eye, heart, gastrointestinal system) is being investigated. The secretion of OXY and AVP is influenced by changes in body fluid osmolality, blood volume, blood pressure, hypoxia, and stress. Vasopressin interacts with three subtypes of receptors: V1aR, V1bR, and V2R whereas oxytocin activates its own OXTR and V1aR receptors. AVP and OXY receptors are present in several regions of the brain (cortex, hypothalamus, pons, medulla, and cerebellum) and in the peripheral organs (heart, lungs, carotid bodies, kidneys, adrenal glands, pancreas, gastrointestinal tract, ovaries, uterus, thymus). Hypertension, myocardial infarction, and coexisting factors, such as pain and stress, have a significant impact on the secretion of oxytocin and vasopressin and on the expression of their receptors. The inappropriate regulation of oxytocin and vasopressin secretion during ischemia, hypoxia/hypercapnia, inflammation, pain, and stress may play a significant role in the pathogenesis of cardiovascular diseases.

Abstract P059: A A Role of Aminopeptidase A in the Brain on Cardiovascular Regulation of Conscious Rat

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Takuto Nakamura ◽  
Masanobu Yamazato ◽  
Akio Ishida ◽  
Yusuke Ohya
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Drinking Behavior ◽  
Cardiovascular Regulation ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Aminopeptidase A ◽  
The Brain

Objective: Aminopeptidase A (APA) have important role in conversion of Ang II to Ang III. Intravenous APA administration lowers blood pressure in hypertensive rats. In contrast, APA inhibition in the brain lowers blood pressure in hypertensive rats. Therefore APA might have different role on cardiovascular regulation. However, a role of APA and Ang III on cardiovascular regulation especially in the brain has not been fully understood. Our purpose of present study was to investigate a role of APA and Ang III in the brain on cardiovascular regulation in conscious state. Method: 12-13 weeks old Wistar Kyoto rat (WKY) and 12-16 weeks old spontaneously hypertensive rat (SHR) were used. i) APA distribution in the brain was evaluated by immunohistochemistry. Protein expression of APA was evaluated by Western blotting. Enzymatic activity of APA was evaluated using L-glutamic acid γ-(4-nitroanilide) as a substrate. ii) WKY received icv administration of Ang II 25ng/2μL and Ang III 25ng/2μL. We recorded change in mean arterial pressure (MAP) in conscious and unrestraied state and measured induced drinking time. iii) SHR received icv administeration of recombinant APA 400ng/4μL. We recorded change in MAP in conscious and unrestraied state and measured induced drinking time. Result: i) APA was diffusely immunostained in the cells of brain stem including cardiovascular regulatory area such as rostral ventrolateral medulla. Protein expression and APA activity in the brain were similar between WKY (n=3) and SHR (n=3).ii) Icv administration of Ang II increased MAP by 33.8±3.8 mmHg and induced drinking behavior for 405±90 seconds (n=4). Icv administration of Ang III also increased MAP by 24.7±2.4 mmHg and induced drinking behavior for 258±62 seconds (n=3). These vasopressor activity and induced drinking behavior was completely blocked by pretretment of angiotensin receptor type 1 blocker.iii) Icv administration of APA increased MAP by 10.0±1.7 mmHg (n=3). Conclusion: These results suggested that Ang III in the brain increase blood pressure by Angiotensin type 1 receptor dependent mechanism and APA in the brain may involved in blood pressure regulation as a vasopressor enzyme.

scholarly journals The concentration of ascorbic acid in the cerebral cortex and internal organs of rats in chronic and acute hyperglycemia

1998 ◽  
Vol 44 (1) ◽  
pp. 40-42
Author(s):  
I. P. Grigoriev
Keyword(s):  
Ascorbic Acid ◽  
Brain Cortex ◽  
Mental Disease ◽  
Streptozotocin Diabetes ◽  
Causative Role ◽  
Internal Organs ◽  
Acute Hyperglycemia ◽  
Acute Hypoglycemia ◽  
The Brain

The author hypothesizes a probable causative role of alteration of ascorbic acid concentration in the brain in the development of mental disease in diabetics. In order to verify this hypothesis, ascorbic acid was measured in the brain cortex of rats 21 days after induction of streptozotocin diabetes or 1 h after intraperitoneal injection of glucose in a dose of 5 g/kg. Ascorbic acid level was increased both in diabetes (456+26 yg/g tissue versus 415+37 \vg/g in the control, p<0.01) and in acute hyperglycemia (475+54 \tg/g versus 406+65 \xg/g in the control, p<0.001). This confirmed that changed concentration of ascorbic acid in the brain can promote the development of a mental disease in diabetics. In the liver the concentration of ascorbic acid was decreased in streptozotocin diabetes (by 17%), p<0.001) and increased in acute hypoglycemia (by 24%, p<0.01). The findings permit us to hypothesize that hypoglycemia inhibits the production of ascorbic acid from the liver to the blood in rats and impedes the transport of ascorbic acid through the gut wall into the blood in humans.

Abstract P152: Aminopeptidase A in the Brain Exerts Cardiovascular Action via Degradation of Kallidin to Bradykinin

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Takuto Nakamura ◽  
Masanobu Yamazato ◽  
Yusuke Ohya
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Cardiovascular Regulation ◽  
Receptor Blocker ◽  
Ang Ii ◽  
Aminopeptidase A ◽  
Hoe 140 ◽  
Wistar Kyoto ◽  
The Brain

Objective: Aminopeptidase A (APA) degrades of various sympathomodulatory peptides such as angiotensin (Ang) II, cholecystkinin-8, neurokinin B and kallidin. APA activity is increased in the brain of hypertensive rats. A centrally acting APA inhibitor prodrug is currently under investigation in clinical trial for treatment of hypertension. In previous reports, a role of APA in the brain on cardiovascular regulation was researched focus on only renin-angiotensin system. We previously reported that intracerebroventricular(icv) administration of APA increased blood pressure and that this pressor response was partially blocked by angiotensin receptor blocker. In this study, we evaluated a role of APA on cardiovascular regulation focusing on peptides other than Ang II. Method: Eleven weeks old Wistar Kyoto rats were used. We icv administrated 800 ng/8 μL of APA after pretreatment of following drugs, i) 8μL of artificial cerebrospinal fluid (aCSF) as a control, ii) 80 nmol/8 μL of amastatin which is a non-specific aminopeptidase inhibitor, iii) 1 nmol/8 μL of HOE-140 which is a bradykinin receptor blocker to evaluate the involvement of degradation of kallidin to bradykinin by APA. Result: i) Icv administration of APA after pretreatment of aCSF increased blood pressure rapidly. Blood pressure reached a peak within 1 minute. The elevated blood pressure decreased gradually and reached baseline blood pressure in 10 minutes. A peak pressor response is 25.5±1.4 mmHg (n=5). ii) Icv pretreatment of amastatin or HOE-140 did not change the blood pressure. A peak pressor response induced by APA is 13.1±4.1 mmHg (n=6, p<0.05 vs aCSF). iii) Icv pretreatment of HOE-140 did not change the blood pressure. A peak pressor response induced by APA is 21.2±1.8 mmHg (n=4, p<0.05 vs aCSF). Conclusion: 1) Icv administration of APA increased blood pressure by APA enzymatic activity. 2) Cardiovascular regulation of APA in the brain is due to not only degradation of Ang II to Ang III but also degradation of kallidin to bradykinin. Clinical implication: We think inhibition of APA in the brain may be a unique therapeutic target which affects several cardiovascular peptides in the brain.

Physiological and pharmacologic effects on TH activity in rabbit and cat carotid body

1981 ◽  
Vol 240 (1) ◽  
pp. R38-R43 ◽  
Author(s):  
C. Gonzalez ◽  
Y. Kwok ◽  
J. Gibb ◽  
S. Fidone
Keyword(s):  
Carotid Body ◽  
Species Differences ◽  
Adrenal Glands ◽  
Catecholamine Biosynthesis ◽  
Carotid Bodies ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
Rate Limiting

The carotid bodies, along with the superior cervical ganglia and the adrenal glands, were removed from rabbits and cats and the activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, was assayed by the method of Nagatsu (Anal. Biochem. 9: 122-126, 1964). The activities of the enzyme, in nmols tyrosine hydroxylated x h-1 x mg tissue-1, were: carotid body, rabbit 1.29, cat 0.84; superior cervical ganglion, rabbit 8.66, cat 4.97; adrenal gland, rabbit 0.95, cat 2.25. With respect to the carotid body, each of the following experimental procedures resulted in a long-term increase in TH activity in the rabbit but not in the cat: 1) severe hypoxia (5% O2 in N2 for 1 h, assay of TH 48 h later); 2) chronic transection of the carotid sinus nerve (assay of TH at 12-15 days); or 3) administration of reserpine (10 mg/kg at 0 and 24 h, assay of TH at 48 h). These observations are compared with our previous findings for rat carotid body and are discussed in relation to the role of catecholamines in chemoreception, and, in particular, to the reported differences in dopamine action in the carotid bodies of these different species. Our results also suggest species differences with respect to the participation of the sympathoadrenal system in response to reserpine and hypoxic stress.

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