Hemodynamic and hormonal responses to hemorrhage in conscious rabbits at mid- and late gestation

1998 ◽  
Vol 275 (4) ◽  
pp. R1082-R1090 ◽  
Author(s):  
Virginia L. Brooks ◽  
Rebecca R. Quesnell ◽  
Colleen M. Kane ◽  
Lanny C. Keil
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Plasma Renin ◽  
Late Gestation ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Hormonal Responses ◽  
Conscious Rabbits ◽  
The Relationship ◽  
Arterial Pressure Regulation

This study tests the hypothesis that conscious rabbits late in pregnancy (P), but not at midgestation (MP), are less able to maintain arterial pressure during hemorrhage. Blood volume (BV) was elevated ( P < 0.05) by an average of 13 ± 4 (MP) and 35 ± 3% (P). Rabbits were bled in both the nonpregnant (NP) and P state at 2% of the initial BV per minute. The hemorrhage was stopped after arterial pressure decreased. In NP rabbits, arterial pressure was well maintained near control pressures of 70 ± 2 mmHg until 38 ± 2% of the initial BV was removed and then rapidly fell to reach a nadir at 35 ± 2 mmHg. In contrast, in P rabbits, basal arterial pressure was lower (61 ± 2 mmHg; P < 0.05) and gradually decreased to below control after <25% of the initial BV was removed. Moreover, the rapid hypotensive phase was triggered with a lower percent BV removal (33 ± 2%; P < 0.05). Basal heart rate was higher during P (149 ± 5 vs. 189 ± 9 beats/min; P < 0.05), and reflex increases were delayed. The slope of the relationship between arterial pressure and vasopressin was not modified during P, although the line was shifted to a lower pressure ( P < 0.05). Larger increases in plasma renin activity and ANG II concentration were produced during hemorrhage in P rabbits. In contrast, no differences in the changes in arterial pressure, heart rate, and vasopressin were found between NP and MP rabbits during hemorrhage, although increases in renin and ANG II were greater at MP ( P < 0.05). In summary, although P conscious rabbits are less able to maintain blood pressure during hemorrhage, this change is not evident at MP. These data suggest that the factors that mediate the P-induced alterations in arterial pressure regulation are not operative until late in gestation.

Hemorrhage decreases arterial pressure sooner in pregnant compared with nonpregnant dogs: role of baroreflex

1994 ◽  
Vol 266 (4) ◽  
pp. H1610-H1619 ◽  
Author(s):  
V. L. Brooks ◽  
L. C. Keil
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Cortisol Concentration ◽  
Right Atrial ◽  
Ang Ii ◽  
The Relationship ◽  
Initial Blood

This study was performed to test the hypothesis that smaller reflex increases in vasopressin, cortisol, adrenocorticotropic hormone (ACTH), and angiotensin II (ANG II) concentrations are produced by hemorrhage in pregnant compared with nonpregnant conscious dogs. Equivalent hemorrhages (1% of the initial blood volume per minute) produced larger decreases in arterial pressure [P < 0.01; 107 +/- 6 to 73 +/- 10 mmHg (pregnant); 109 +/- 6 to 90 +/- 5 mmHg (nonpregnant)] but produced similar increases in plasma vasopressin concentration in the pregnant animals. As a result, the slope of the arterial pressure-to-vasopressin relationship was reduced (P < 0.05). During pregnancy, smaller increases in plasma cortisol concentration and heart rate were also produced for a given decrease in arterial pressure, but the relationship between pressure and ACTH was not significantly affected. In contrast, higher levels of plasma renin activity and plasma ANG II concentration were achieved in the pregnant dogs. In general, the relationships between plasma hormone levels and either left or right atrial pressure were not significantly altered. These results indicate that reflex increases in heart rate, vasopressin, and cortisol concentration are attenuated in pregnant dogs and that this attenuation may contribute to the inability of pregnant animals to achieve normal cardiovascular homeostasis during hemorrhage.

The arterial depressor response to chronic low-dose angiotensin II infusion in female rats is estrogen dependent

2012 ◽  
Vol 302 (1) ◽  
pp. R159-R165 ◽  
Author(s):  
Amanda K. Sampson ◽  
Lucinda M. Hilliard ◽  
Karen M. Moritz ◽  
Merlin C. Thomas ◽  
Chris Tikellis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Low Dose ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Estrogen Replacement ◽  
Sprague Dawley ◽  
Arterial Pressure Regulation

The complex role of the renin-angiotensin-system (RAS) in arterial pressure regulation has been well documented. Recently, we demonstrated that chronic low-dose angiotensin II (ANG II) infusion decreases arterial pressure in female rats via an AT2R-mediated mechanism. Estrogen can differentially regulate components of the RAS and is known to influence arterial pressure regulation. We hypothesized that AT2R-mediated depressor effects evident in females were estrogen dependent and thus would be abolished by ovariectomy and restored by estrogen replacement. Female Sprague-Dawley rats underwent ovariectomy or sham surgery and were treated with 17β-estradiol or placebo. Mean arterial pressure (MAP) was measured via telemetry in response to a 2-wk infusion of ANG II (50 ng·kg−1·min−1 sc) or saline. MAP significantly decreased in females treated with ANG II (−10 ± 2 mmHg), a response that was abolished by ovariectomy (+4 ± 2 mmHg) and restored with estrogen replacement (−6 ± 2 mmHg). Cardiac and renal gene expression of components of the RAS was differentially regulated by estrogen, such that overall, estrogen shifted the balance of the RAS toward the vasodilatory axis. In conclusion, estrogen-dependent mechanisms offset the vasopressor actions of ANG II by enhancing RAS vasodilator pathways in females. This highlights the potential for these vasodilator pathways as therapeutic targets, particularly in women.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Effect of vasopressin blockade on blood pressure during water deprivation in intact and baroreceptor-denervated conscious dogs

1988 ◽  
Vol 254 (4) ◽  
pp. E490-E495 ◽  
Author(s):  
L. C. Gregory ◽  
E. W. Quillen ◽  
L. C. Keil ◽  
D. Chang ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation ◽  
Marked Contrast

Previous studies have provided evidence that vasopressin plays an important role in blood pressure regulation during water deprivation. However, these investigations have been complicated by reflex compensatory increases in cardiac output and renin secretion. The aim of the present study was to investigate the effect of blockade of the vasoconstrictor action of vasopressin in conscious water-deprived dogs in which the low- and/or high-pressure baroreceptors were denervated to minimize reflex responses. Vasopressin blockade in sham-operated dogs (n = 7) did not change arterial pressure. Heart rate rose from 78 +/- 9 to 119 +/- 13 beats/min (P less than 0.01), and plasma renin activity increased from 10.9 +/- 2.1 to 21.6 +/- 4.6 ng.ml-1.3 h-1 (P less than 0.01). In carotid sinus-denervated dogs (n = 6), vasopressin blockade again failed to decrease arterial pressure. Heart rate increased from 105 +/- 10 to 132 +/- 10 beats/min (P less than 0.01), and plasma renin activity rose from 6.8 +/- 1.7 to 15.5 +/- 2.4 ng.ml-1.3 h-1 (P less than 0.01). The antagonist also failed to change blood pressure in cardiac-denervated dogs (n = 5). Heart rate increased from 111 +/- 9 to 119 +/- 1 beats/min (P less than 0.01), but plasma renin activity did not increase significantly. In marked contrast, vasopressin blockade in sinoaortic/cardiac-denervated dogs (n = 7) promptly decreased arterial pressure from 115 +/- 8 to 94 +/- 7 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Insulin-regulated aminopeptidase deficiency impairs cardiovascular adaptations and placental development during pregnancy

2020 ◽  
Vol 134 (23) ◽  
pp. 3213-3228
Author(s):  
Sarah L. Walton ◽  
Katrina M. Mirabito Colafella ◽  
Aneesa Ansari ◽  
Siew Yeen Chai ◽  
Kate M. Denton
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Knockout Mice ◽  
Late Gestation ◽  
Wild Type ◽  
Placental Development ◽  
Junctional Zone ◽  
Fluid Handling ◽  
Arterial Pressure Regulation

Abstract Insulin-regulated aminopeptidase (IRAP), an enzyme that cleaves vasoactive peptides including oxytocin and vasopressin, is suggested to play a role in pregnancy and the onset of preeclampsia. Our aim was to examine the contribution of IRAP to arterial pressure regulation and placental development during pregnancy in mice. Mean arterial pressure and heart rate were measured via radiotelemetry in 12-week-old female wild-type and IRAP knockout mice. Females were time-mated with males of the same genotype. Placentae were collected at embryonic day 18.5 for histological analysis. Basal heart rate was ∼40 bpm lower in IRAP knockout females compared with wild-type females. The increase in heart rate across gestation was greater in IRAP knockout females than wild-type females. Neither basal nor gestational mean arterial pressure was different between wildtype and IRAP knockout females. Urine output and water intake of IRAP knockout mice were ∼45% less than wild-type mice at late gestation. IRAP deficiency had no effect on fetal weight. Morphological assessment of placentae revealed that IRAP deficiency was associated with reduced labyrinth surface area and accumulation of glycogen in the junctional zone. Our data demonstrate that IRAP deficiency alters maternal fluid handling and impairs placental labyrinth expansion at late gestation, indicating that IRAP contributes to the normal adaptions to pregnancy.

Comparative actions of adrenomedullin and nitroprusside: interactions with ANG II and norepinephrine

2001 ◽  
Vol 281 (6) ◽  
pp. R1887-R1894 ◽  
Author(s):  
Christopher J. Charles ◽  
M. Gary Nicholls ◽  
Miriam T. Rademaker ◽  
A. Mark Richards
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Biological Responses ◽  
Conscious Sheep

The role of adrenomedullin (ADM) in volume and pressure homeostasis remains undefined. Accordingly, we compared the biological responses to infusions of ADM and nitroprusside (NP; matched for reduction of arterial pressure) and assessed their effects on responses to ANG II and norepinephrine in eight conscious sheep. During matched falls in arterial pressure (8–10 mmHg, both P < 0.001) ADM and NP induced similar increases in heart rate. ADM increased cardiac output ( P < 0.001), and the fall in calculated peripheral resistance was greater with ADM than NP ( P = 0.013). ADM infusions raised plasma ADM levels ( P < 0.001), plasma renin activity ( P = 0.001), and ANG II ( P < 0.001) but tended to blunt any concurrent rise in aldosterone compared with NP ( P = 0.056). ADM maintained both urine flow ( P < 0.001) and sodium excretion ( P = 0.01) compared with falls observed with NP. ADM attenuated the vasopressor actions of exogenous ANG II ( P = 0.006) but not norepinephrine. In addition, ADM antagonized the ANG II-induced rise in plasma aldosterone ( P < 0.001). In conclusion, ADM induces a different spectrum of hemodynamic, renal, and endocrine actions to NP. These results clarify mechanisms by which ADM might contribute to volume and pressure homeostasis.

scholarly journals Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1703-R1711 ◽  
Author(s):  
Yasufumi Nakajima ◽  
Hiroshi Nose ◽  
Akira Takamata
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Skin Blood Flow ◽  
Plasma Osmolality ◽  
Cardiovascular Responses ◽  
Pressure Regulation ◽  
Highly Correlated ◽  
Arterial Pressure Regulation

To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (ΔPV) = −20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (ΔPosm) = 23 mosmol/kgH2O, ΔPV = −16%], and hypovolemic and more hyperosmotic (HL2, ΔPosm = 52 mosmol/kgH2O, ΔPV = −17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35°C air temperature, ∼20% relative humidity) for 1–2 h until rectal temperatures (Tre) reached 40.0°C. Mean arterial pressure in L decreased with rise in Tre( P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to ∼30% of that in C ( P < 0.001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Trethreshold for TVD was highly correlated with Posm( r = 0.94, P < 0.001). Heart rate in the HL groups increased with rise in Tre( P < 0.001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.

Sign in / Sign up

Export Citation Format

Share Document