scholarly journals Vandy - Tail-Cuff Blood Pressure v1 (protocols.io.yymfxu6)

protocols.io ◽  
2019 ◽  
Author(s):  
Chee Lim
Keyword(s):  
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Trevor Chan ◽  
Rajesh Dash ◽  
Paul C Simpson

Background: Alpha-1-adrenergic receptor (AR) agonists classically increase blood pressure (BP). Among the 3 alpha-1-AR subtypes, A, B, and D, the alpha-1A is required for cardiac protection in a knockout (KO) mouse, and is sufficient for protection of cultured cardiac myocytes, via ERK activation. However, it is unknown if activation of the alpha-1A-subtype by a drug can protect the heart in vivo. Hypothesis: At a dose that does not increase BP, an agonist selective for the alpha-1A-AR subtype can prevent cardiomyopathy. Methods: We gave the alpha-1A agonist A61603 (A6) to 11 week-old wild type (WT) male C57Bl6J mice by osmotic minipump. We induced cardiomyopathy with a single dose of doxorubicin (DOX) (25 mg/kg IP), a cardiotoxic cancer drug. We measured BP by tail cuff, activated (phosphorylated, P)-ERK by immunoblot, heart mRNAs by RT-qPCR, fractional shortening (FS) by echocardiog-raphy (ECHO), myocyte necrosis by serum creatine kinase (CK), apoptosis by TUNEL stain, and fibrosis by sirius red stain. Results : In dose-finding experiments (0.01–100 ug/kg/d), A6 at 10 ng/kg/d over 7 days had no effect on daily tail cuff BP (average mmHg Vehicle 115 ± 4; A6 119 ± 4), but increased heart P-ERK (1.7-fold) and the mRNAs for beta-MyHC and ANF (5-fold). A6 at higher doses increased BP. Next, A6 at the non-hypertensive dose (10 ng/kg/d) or vehicle was infused over 7 days after a single DOX injection. The TABLE shows that DOX caused cardiomyopathy, with reduced survival and FS, and increased necrosis, apoptosis, and fibrosis (data are mean ± SE). A6 prevented all of these abnormalities. In alpha-1A-subtype KO mice, DOX caused increased apoptosis and mortality compared with WT mice, and A6 had no beneficial effect (not shown), indicating specificity of A6. Conclusions: A very low dose of an agonist selective for the alpha-1A-AR subtype can activate cardiac survival signaling (P-ERK), induce cardiac fetal genes, and prevent DOX-induced cardiomyopathy, all without increasing BP.


Biomedicines ◽  
2020 ◽  
Vol 8 (10) ◽  
pp. 424
Author(s):  
Perla Y. Gutiérrez-Arzapalo ◽  
Pilar Rodríguez-Rodríguez ◽  
David Ramiro-Cortijo ◽  
Marta Gil-Ortega ◽  
Beatriz Somoza ◽  
...  

Fetal undernutrition programs hypertension and cardiovascular diseases, and resistance artery remodeling may be a contributing factor. We aimed to assess if fetal undernutrition induces resistance artery remodeling and the relationship with hypertension. Sprague–Dawley dams were fed ad libitum (Control) or with 50% of control intake between days 11 and 21 of gestation (maternal undernutrition, MUN). In six-month-old male and female offspring we assessed blood pressure (anesthetized and tail-cuff); mesenteric resistance artery (MRA) structure and mechanics (pressure myography), cellular and internal elastic lamina (IEL) organization (confocal microscopy) and plasma MMP-2 and MMP-9 activity (zymography). Systolic blood pressure (SBP, tail-cuff) and plasma MMP activity were assessed in 18-month-old rats. At the age of six months MUN males exhibited significantly higher blood pressure (anesthetized or tail-cuff) and plasma MMP-9 activity, while MUN females did not exhibit significant differences, compared to sex-matched controls. MRA from 6-month-old MUN males and females showed a smaller diameter, reduced adventitial, smooth muscle cell density and IEL fenestra area, and a leftward shift of stress-strain curves. At the age of eighteen months SBP and MMP-9 activity were higher in both MUN males and females, compared to sex-matched controls. These data suggest that fetal undernutrition induces MRA inward eutrophic remodeling and stiffness in both sexes, independent of blood pressure level. Resistance artery structural and mechanical alterations can participate in the development of hypertension in aged females and may contribute to adverse cardiovascular events associated with low birth weight in both sexes.


2004 ◽  
Vol 286 (6) ◽  
pp. H2408-H2415 ◽  
Author(s):  
Steven E. Whitesall ◽  
Janet B. Hoff ◽  
Alan P. Vollmer ◽  
Louis G. D'Alecy

Radiotelemetry of mouse blood pressure accurately monitors systolic pressure, diastolic pressure, heart rate, and locomotor activity but requires surgical implantation. Noninvasive measurements of indirect systolic blood pressure have long been available for larger rodents and now are being reported more frequently for mice. This study compared mouse systolic arterial blood pressure measurements using implanted radiotelemetry pressure transducer with simultaneous tail-cuff measurements in the same unanesthetized mice. The pressure range for comparison was extended by inducing experimental hypertension or by observations of circadian elevations between 3 AM and 6 AM. Both trained and untrained tail-cuff operators used both instruments. Every effort was made to follow recommended manufacturer's instructions. With the initial flow-based tail-cuff instrument, we made 671 comparisons (89 sessions) and found the slope of the linear regression to be 0.118, suggesting poor agreement. In an independent assessment, 277 comparisons (35 sessions) of radiotelemetry measurements with the pulse based tail-cuff instrument were made. The slope of the linear regression of the simultaneous measurements of systolic pressures was 0.98, suggesting agreement. Bland-Altman analysis also supported our interpretation of the linear regression. Thus although reliable systolic pressure measurements are possible with either tail-cuff or radiotelemetry techniques, in our hands some tail-cuff instruments fail to accurately detect elevated blood pressures. These data, however, do not distinguish whether this instrument-specific tail-cuff failure was due to operator or instrument inadequacies. We strongly advise investigators to obtain an independent and simultaneous validation of tail-cuff determinations of mouse blood pressure before making critical genotyping determinations.


1993 ◽  
Vol 66 (2) ◽  
pp. 147-155 ◽  
Author(s):  
C.S. Godin ◽  
E.C. Kimmel ◽  
J.M. Drerup ◽  
H.F. Leahy ◽  
D.L. Pollard

2007 ◽  
Vol 293 (1) ◽  
pp. F139-F147 ◽  
Author(s):  
Rudy M. Ortiz ◽  
Miguel L. Graciano ◽  
Dale Seth ◽  
Mouhamed S. Awayda ◽  
L. Gabriel Navar

Effects of aldosterone receptor (AR) blockade with eplerenone (epl) on renal Na+ excretion, arterial blood pressure, intra-adrenal and renal ANG II, and plasma aldosterone levels during ANG II-dependent hypertension were evaluated. Rats from one cohort ( n = 10/group) 1) control, 2) control + epl (25 mg/day), 3) ANG II (60 ng/min), and 4) ANG II + epl were maintained in metabolic cages for 28 days for daily urine collections. Systolic blood pressure (SBP) was measured weekly by tail-cuff. In a second cohort ( n = 12/group), daily SBP was measured by telemetry ( n = 6 rats/group) 1) control, 2) ANG II, and 3) ANG II + epl. A diet containing epl (0.1%) was provided after 1 wk of ANG II infusion. Direct monitoring of BP by telemetry showed that epl delayed the onset of the increase in SBP by 2 days and slightly reduced SBP (186 ± 6 vs. 177 ± 8 mmHg). Epl transiently increased Na+ excretion within 24 h of treatment in both normo- and hypertensive rats; however, balance was reestablished within 5 days suggesting that alternative mechanisms for conserving Na+ are activated. Cortical α-epithelial Na+ channel content (α-ENaC) was not altered after 21 days of epl treatment. Epl exacerbated the ANG II-mediated increases in intrarenal ANG II (226 ± 16 vs. 365 ± 38 fmol/g) and further increased intra-adrenal ANG II (3.9 ± 0.3 vs. 8.2 ± 0.9 fmol/mg) and aldosterone (255 ± 55 vs. 710 ± 87 pmol/mg) content. Exacerbation of intrarenal ANG II levels likely contributes to the maintenance of α-ENaC protein content and thus Na+ reabsorption, which helps explain the ineffectiveness of AR blockade in reducing SBP in ANG II-infused models of hypertension.


1975 ◽  
Vol 14 (5) ◽  
pp. 659-662 ◽  
Author(s):  
Joseph B. Sia ◽  
Elias Schwam ◽  
William Mann ◽  
Jerry Sepinwall

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