Cold stress causes intense sympathoexcitation, producing a tachycardic and pressor response, and an increase in MSNA (32, 33). The pressor response is due to an initial rise in CO, in response to increased HR and a later increase in MSNA, causing vasoconstriction. Both MAP and TPR show a linear correlation with MSNA during cold stress (34). In our study, cold stress produced a pressor response in both groups, but, interestingly, while SBP and MAP continued to rise with placebo throughout the test period, the pressor response to cold was blunted in subjects who had taken CBD, and SBP and MAP were significantly lower. In keeping with this, TPR was lower with CBD than placebo, suggesting a possible inhibition of sympathetic outflow. This could also be due to analgesic properties of CBD (35), reducing cold stress and therefore minimizing the sympathetic response (also explaining why the cold pressor test was affected more by CBD than the exercise test). In the animal study of Resstel and colleagues (13), the authors suggested that the modulation of cardiovascular response was most likely secondary to attenuation of emotional response to stress. However, given our findings that CBD produced similar changes in cardiovascular parameters — though to a variable degree — during rest and stress, this may indicate that CBD also has direct cardiovascular effects.
CBD may cause sympathoinhibition (through CB1 or some other mechanism), thereby preventing an increase in blood pressure and cardiac output, causing a compensatory rise in heart rate to maintain cardiac output. Indeed, the changes in SBP preceded any changes in HR. Another possibility is that CBD inhibits cardiac vagal tone, thereby increasing heart rate (despite any potential sympathoinhibition). A recent study in male Sprague-Dawley rats showed that GPR18 activation in the rostral ventrolateral medulla (RVLM) by abnormal CBD (Abn-CBD) resulted in reduced blood pressure and increased heart rate (23) (similar to that observed in the present study). The same study showed that pretreatment with atropine and propranolol fully abrogated the HR response, suggesting a role for the autonomic nervous system. CBD is a weak partial agonist at GPR18 (24).
During an initial visit, subjects were familiarized with the stress tests and with noninvasive cardiovascular (CVS) monitoring, and an electrocardiogram (ECG) was done to rule out any preexisting cardiac conditions. Subjects were advised to fast overnight, to avoid beverages containing caffeine or alcohol, and to avoid strenuous exercise for 24 hours before each of the 2 study visits. Two hours after CBD/placebo was administered, subjects performed various stress tests (36). Noninvasive cardiovascular monitoring using Finometer and laser Doppler flowmetry was carried out during the 2 hours to assess changes in baseline parameters and during the stress test periods.
METHODS. Nine healthy male volunteers were given 600 mg of CBD or placebo in a randomized, placebo-controlled, double-blind, crossover study. Cardiovascular parameters were monitored using a finometer and laser Doppler.
Mental stress caused a rise in HR (P < 0.05; Figure 3D ) and a decline in SV (P < 0.01; Figure 3E ), which was seen in both the CBD and placebo groups. There was a rise in DBP (P < 0.05; Figure 3B ) and a decline in EJT (P < 0.05; Figure 3G ), seen only in those who had taken CBD.
Cannabinoids (CBs) are compounds that bind to CB receptors or are structurally similar to compounds that bind to CB receptors. They include endogenously produced compounds (called endocannabinoids), synthetic compounds and phytocannabinoids obtained from the Cannabis sativa plant. There are over 80 known types of phytocannabinoids, the most widely studied of which is Δ 9 tetrahydrocannabinol (Δ 9 -THC or THC), which is responsible for the psychoactive properties of cannabis (4). The other major phytocannabinoid is cannabidiol (CBD), which does not have psychoactive properties. CBD is currently the focus of much research due to its potential in a number of therapeutic areas, as it has been shown to have antiinflammatory, anticonvulsant, antioxidant, anxiolytic, antinausea, and antipsychotic properties (5). A number of preclinical studies have also shown beneficial effects of CBD in a range of disorders of the cardiovascular system (6). A CBD/THC combination (Sativex/Nabiximols, GW Pharmaceuticals) is licensed for the treatment of spasticity in multiple sclerosis, and CBD alone (Epidiolex, GW Pharmaceuticals) has entered an expanded access program in children with intractable epilepsies (Dravet syndrome and Lennox-Gastaut syndrome). Epidiolex has also received orphan designation status for the treatment of neonatal hypoxia-ischaemic encephalopathy.
The effects of placebo (closed square) and CBD (open square) on systolic blood pressure (SBP) (A), diastolic blood pressure (DBP) (B), mean arterial blood pressure (MAP) (C), heart rate (HR) (D), stroke volume (SV) (E), cardiac output (CO) (F), ejection time (EJT) (G), total peripheral resistance (TPR) (H), and forearm blood flow (I), measured continuously just before, during, and after cold pressor test (dotted line denotes stress test period), except for forearm blood flow. Measurements for forearm blood flow were made over a 2-minute window just before, during, and after the stress test. Repeated measures 2-way ANOVA; mean ± SEM (*/ + / # P < 0.05, **/ ++ P < 0.01, ***/ +++ P < 0.001, ****P < 0.0001 using Bonferroni post-hoc analysis; + and # denote significant change in a parameter during the stress period seen with placebo and CBD, respectively).
Although overall, there was no difference in the cardiovascular parameters between the 2 treatments, post-hoc analysis showed that SBP ( Figure 3A ; P < 0.05 to < 0.0001), DBP ( Figure 3B ; P < 0.05 to < 0.01), and MAP ( Figure 3C ; P < 0.05 to < 0.0001) were significantly lower in volunteers who had taken CBD, especially immediately after the stress test. Looking at the individual response to mental stress, 6 of 9 subjects had a lower SBP before or during the mental stress test, and 9 of 9 subject had a lower SBP in the recovery period after taking CBD ( Figure 2 ). Five of 9 subjects had a lower DBP during the mental stress test, and 6 of 9 subject had a lower DBP in the recovery period after taking CBD ( Figure 2 ).
GT is supported by the NIHR Oxford Biomedical Research Centre Programme. The views expressed are those of the author and not necessarily those of the NHS, the NIHR, or the Department of Health.
With high blood pressure you should look at what can be done on the front end of the problem. No medication or supplement is better for your heart and arteries than clean living. But if you already have high blood pressure, and you want to remedy the symptoms, then you can take certain medications.
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We want to give the reader as simple an answer as possible, and a direct one. But because we’re dealing with a serious medical issue that can have dire outcomes, we want to be extremely careful.
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We looked into the science behind the research, and took a serious eye to whether there’s any indication that CBD actually works for high blood pressure. Then we reviewed five CBD products that we picked for their specific benefits. If you still have questions at the end, please check out the FAQs
People all over the world are taking CBD. And they’re finding new applications of the supplement almost every year. Cannabidiol, or CBD, has recently been researched for use by people with high blood pressure.
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Now we look at what has caused the high blood pressure to see what CBD can do to alleviate the symptoms. The not-so-good news is that we didn’t find a lot of evidence to support CBD treating plaque in arteries or any blood clotting issues. That means that if your high blood pressure is due to either of those causes, CBD may not be the remedy for you.
To begin with, we should talk for a quick moment about the difference between preventative medicine and remedial medicine. An easy example of the difference is our diet. If we eat less fat and sugar, that’s preventative. If we don’t change our diet, we need to exercise more, which is remedial, or “of a remedy.”