Hemodynamic Responses Elicited By γ2-MSH or Blood Replacement in Hemorrhaged Rats

Whalen, Erin J.; Lewis, Stephen J.; Johnson, Alan Kim

doi:10.1016/j.jss.2006.09.025

Cited by 2 publications

(4 citation statements)

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“…The withdrawal of slightly larger amounts of blood (5.9 ± 0.5 ml) in rats that were to receive injections of H-saline resulted in similar hemodynamic responses. It should be noted that these HEM-induced hemodynamic responses were similar to those we have reported previously (Whalen et al, 2007) and that despite the relatively greater prior withdrawal of blood, the administration of H-saline elicited a marked improvement of resting MAP (see below). The withdrawal of blood (6.2 ± 0.5 ml) in rats that were to receive injections of I-saline, elicited similar initial falls in MAP and HR to the above groups.…”

Section: Discussionsupporting

confidence: 88%

“…As such, it is likely that the beneficial actions of H-saline in our study also involved changes in the activities of AV3V neurons that control neurogenic outflow and the release of hormones regulating vascular tone and fluid/salt balance such as angiotensin II and arginine vasopressin (see Barbosa et al, 1990, 1992). It should be mentioned that systemic injections of γ 2 -melanocyte-stimulating hormone (γ 2 -MSH) elicits equivalent increases in resistance in the renal, mesenteric and hindquarter vascular beds of pentobarbital-anesthetized rats (Whalen et al, 2007). Since, systemic injections of γ 2 -MSH elicits pressor responses primarily via centrally-mediated increases in sympathetic drive and direct vasoconstriction in the renal microcirculation (see Whalen et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…It should be mentioned that systemic injections of γ 2 -melanocyte-stimulating hormone (γ 2 -MSH) elicits equivalent increases in resistance in the renal, mesenteric and hindquarter vascular beds of pentobarbital-anesthetized rats (Whalen et al, 2007). Since, systemic injections of γ 2 -MSH elicits pressor responses primarily via centrally-mediated increases in sympathetic drive and direct vasoconstriction in the renal microcirculation (see Whalen et al, 2007). it is evident that sympathetic effector mechanisms can be effectively stimulated in HEM rats.…”

Section: Discussionmentioning

confidence: 99%

“…However, although the changes in systemic vascular resistances during HEM in animals have received attention (see Liu et al, 2003; Whalen et al, 2007), nothing is known about the changes in systemic resistances elicited by administration of I-saline or H-saline in these rats. Such vital data would help us to understand how vascular beds subserving different physiological roles respond to HEM and to H-saline.…”

Section: Introductionmentioning

confidence: 99%

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Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Whalen

Johnson

Lewis

2014

Microvascular Research

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Purpose The objectives of this study were (i) to characterize the hemodynamic responses caused by controlled hemorrhage (HEM) in pentobarbital-anesthetized rats, and (ii) to determine the responses elicited by systemic bolus injections of isotonic saline (0.15 M) or hypertonic saline (3 M) given 5 min after completion of HEM. Results Controlled HEM (4.3 ± 0.2 ml/rat at 1.5 ml/ min) resulted in a pronounced and sustained fall in mean arterial blood pressure (MAP) to about 40 mmHg. The fall in MAP was associated with a reduction in hindquarter vascular resistance (HQR) but no changes in renal (RR) or mesenteric (MR) vascular resistances. Systemic injections of isotonic saline (96–212 µmol/kg iv, in 250–550 µl) did not produce immediate responses but promoted the recovery of MAP to levels below pre-HEM values. Systemic injections of hypertonic saline (750–3000 µmol/kg, i.v., in 250–550 µl) produced immediate and pronounced falls in MAP, RR, MR and especially HQR of 30–120 sec in duration. However, hypertonic saline prompted a full recovery of MAP, HQR and RR to pre-HEM levels and an increase in MR to levels above pre-HEM values. Conclusions This study demonstrates that (i) HEM induced a pronounced fall in MAP which likely involved a fall in cardiac output and HQR, (ii) isotonic saline did not fully normalize MAP, and (iii) hypertonic saline produced dramatic initial responses, and promoted normalization of MAP probably by restoring blood volume and cardiac output through sequestration of fluid from intracellular compartments.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Whalen

Johnson

Lewis

2014

Microvascular Research

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Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

Zhai

et al. 2022

Oxidative Medicine and Cellular Longevity

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Hemorrhagic shock is associated with activation of renin-angiotensin system (RAS) and endoplasmic reticulum stress (ERS). Previous studies demonstrated that central RAS activation produced by various challenges sensitizes angiotensin (Ang) II-elicited hypertension and that ERS contributes to the development of neurogenic hypertension. The present study investigated whether controlled hemorrhage could sensitize Ang II-elicited hypertension and whether the brain RAS and ERS mediate this sensitization. Results showed that hemorrhaged (HEM) rats had a significantly enhanced hypertensive response to a slow-pressor infusion of Ang II when compared to sham HEM rats. Treatment with either angiotensin-converting enzyme (ACE) 1 inhibitor, captopril, or ACE2 activator, diminazene, abolished the HEM-induced sensitization of hypertension. Treatment with the ERS agonist, tunicamycin, in sham HEM rats also sensitized Ang II-elicited hypertension. However, blockade of ERS with 4-phenylbutyric acid in HEM rats did not alter HEM-elicited sensitization of hypertension. Either HEM or ERS activation produced a greater reduction in BP after ganglionic blockade, upregulated mRNA and protein expression of ACE1 in the hypothalamic paraventricular nucleus (PVN), and elevated plasma levels of Ang II but reduced mRNA expression of the Ang-(1-7) receptor, Mas-R, and did not alter plasma levels of Ang-(1-7). Treatment with captopril or diminazene, but not phenylbutyric acid, reversed these changes. No treatments had effects on PVN protein expression of the ERS marker glucose-regulated protein 78. The results indicate that controlled hemorrhage sensitizes Ang II-elicited hypertension by augmenting RAS prohypertensive actions and reducing RAS antihypertensive effects in the brain, which is independent of ERS mechanism.

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Hemodynamic Responses Elicited By γ2-MSH or Blood Replacement in Hemorrhaged Rats

Cited by 2 publications

References 40 publications

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

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