The cardiovascular responses to ketamine injected intracisternally were examined in chloralose anaesthetized cats. Blood pressure and heart rate were recorded at different time intervals after intracisternal injection of drug or saline vehicle. The low doses of ketamine (0.5 or 1.0 mg) elicited dose dependent increase in blood pressure and heart rate. In contrast the high dose of ketamine (4 mg), produced a fall in blood pressure and heart rate. The cardiovascular response elicited by the low dose was naloxone insensitive and completely blocked by haloperidol, but not by dopamine antagonist pimozide. The vasodepressor and bradycardiac effect of the 4 mg dose was naloxone antagonizable. These data show that excitatory cardiovascular effects of the low dose result from a naloxone resistant site while in high doses an inhibitory effect is elicited by action at naloxone sensitive opiate receptors.
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http://dx.doi.org/10.1007/BF00169042 | DOI Listing |
Hypertens Pregnancy
December 2025
Department of Physiology and Anatomy, University of North Texas Health Science Center, Fort Worth, TX, USA.
Background: Preeclampsia (PE) is characterized as de novo hypertension (HTN) with end-organ damage, especially in the brain. PE is hypothesized to be caused by placental ischemia. PE affects ~5-8% of USA pregnancies and increases the risk for HTN and cerebrovascular diseases (CVD) later in life.
View Article and Find Full Text PDFBMC Pregnancy Childbirth
January 2025
Obstetrics and Gynecology Center, Department of Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, 510280, China.
Background: Preeclampsia, characterized by hypertension and proteinuria during pregnancy, poses significant risks to both mother and fetus. The complement system's aberrant activation, notably the C3AR1, is important to the pathogenesis of preeclampsia, although the precise mechanisms are not fully understood.
Materials And Methods: Utilizing the Comparative Toxicogenomics Database (CTD) and Molecular Signatures Database (MSigDB), we identified complement system targets associated with preeclampsia and environmental pollutants.
Sci Rep
January 2025
Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, NO. 172 Tong Zi Po Road, Yuelu District, Changsha, 410006, Hunan, China.
Osteoporotic fractures are a major public health concern, particularly among the aging population, as they significantly contribute to morbidity, mortality, and reduced quality of life. While cardiovascular health (CVH) has traditionally been linked to cardiovascular disease outcomes, emerging evidence suggests it may also influence bone health. This study investigates the association between CVH, as measured by the Life's Essential 8 (LE8) score, and the prevalence of osteoporotic fractures in U.
View Article and Find Full Text PDFJ Hum Hypertens
January 2025
Research Centre, Montreal Heart Institute, Montreal, QC, Canada.
Age-related arterial stiffness increases pulsatility that reaches the cerebral microcirculation, compromises cerebrovascular health and lead to cognitive decline. The presence of cardiovascular risk factors (CVRFs) such as high blood pressure can exacerbate this effect. Despite extensive research on the impact of antihypertensive treatments on reducing arterial stiffness, little is known about the impact of antihypertensive treatments on pulsatility in cerebral microcirculation.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Pharmacology and Experimental Therapeutics; MS 1015, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, Health Education Building; Room 282E, 3000 Arlington Ave, Toledo, OH, 43614, USA.
We previously demonstrated that the inability of primary endothelial cilia to sense fluid shear stress can lead to nitric oxide (NO) deficiency and cause hypertension (HTN). Decreased biosynthesis of NO contributes to cerebral amyloid angiopathy in Alzheimer's disease (AD) patients through increased deposition of amyloid beta (Aβ). However, the molecular mechanisms underlying the pathogenesis of HTN and AD are incompletely understood.
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