d-arg-dmt-lys-phe-nh2 and Hypertension

d-arg-dmt-lys-phe-nh2 has been researched along with Hypertension* in 2 studies

Reviews

1 review(s) available for d-arg-dmt-lys-phe-nh2 and Hypertension

ArticleYear
Enhancing Mitochondrial Health to Treat Hypertension.
    Current hypertension reports, 2018, 08-17, Volume: 20, Issue:10

    This review summarizes literature pertaining to the dawning field of therapeutic targeting of mitochondria in hypertension and discusses the potential of these interventions to ameliorate hypertension-induced organ damage.. In recent years, mitochondrial dysfunction has been reported as an important contributor to the pathogenesis of hypertension-related renal, cardiac, and vascular disease. This in turn prompted development of novel mitochondria-targeted compounds, some of which have shown promising efficacy in experimental studies and safety in clinical trials. In addition, drugs that do not directly target mitochondria have shown remarkable benefits in preserving these organelles in experimental hypertension. Enhancing mitochondrial health is emerging as a novel feasible approach to treat hypertension. Future perspectives include mechanistic experimental studies to establish a cause-effect relationship between mitochondrial dysfunction and hypertension and further clinical trials to confirm the reno-, cardio-, and vasculo-protective properties of these compounds in hypertension.

    Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Antioxidants; Homeostasis; Humans; Hypertension; Mitochondria; Oligopeptides; Reactive Oxygen Species

2018

Other Studies

1 other study(ies) available for d-arg-dmt-lys-phe-nh2 and Hypertension

ArticleYear
Hypertension Exacerbates Cerebrovascular Oxidative Stress Induced by Mild Traumatic Brain Injury: Protective Effects of the Mitochondria-Targeted Antioxidative Peptide SS-31.
    Journal of neurotrauma, 2019, 12-01, Volume: 36, Issue:23

    Traumatic brain injury (TBI) induces cerebrovascular oxidative stress, which is associated with neurovascular uncoupling, autoregulatory dysfunction, and persisting cognitive decline in both pre-clinical models and patients. However, single mild TBI (mTBI), the most frequent form of brain trauma, increases cerebral generation of reactive oxygen species (ROS) only transiently. We hypothesized that comorbid conditions might exacerbate long-term ROS generation in cerebral arteries after mTBI. Because hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive and spontaneously hypertensive rats (SHR) and assessed changes in cytoplasmic and mitochondrial superoxide (O

    Topics: Animals; Antioxidants; Brain Concussion; Drug Delivery Systems; Hypertension; Male; Mitochondria; Neuroprotective Agents; Oligopeptides; Oxidative Stress; Rats; Rats, Inbred SHR; Rats, Wistar

2019