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For people with controlled high blood pressure, eating a meal with lots of potassium doesn't change how well their blood vessels relax at the start of the meal compared to a meal with less potassium.
Descriptive
When mice eat a lot of salt, adding a moderate amount of potassium lowers their blood pressure, showing that potassium's main benefit might be fighting high blood pressure caused by salt.
In mice eating normal salt, even though extra potassium slows down one salt-handling channel (NCC), it doesn't lower blood pressure because another channel (ENaC) starts pulling in more salt instead.
In mice, when aldosterone hits about 2701 pg/24h (a bit more than normal), the kidney's ENaC channels jump to their highest activity level.
Correlational
When mice eat a lot of salt, their kidney's salt-handling channels (NCC and ENaC) are already low, and adding more potassium doesn't make ENaC any higher.
When mice eat more potassium on normal salt, their kidney's salt-handling channels change: one type (NCC) slows down but another (ENaC) speeds up, especially when aldosterone hits about 2701 pg/24h.
Mechanistic
In mice, more potassium leads to more aldosterone in a straight-line way, but blood pressure rises sharply only when aldosterone hits a certain level (around 4040 pg/24h), then levels off.
When mice eat a lot of salt, adding a moderate amount of potassium lowers their blood pressure by about 3.6 mmHg compared to eating the same high salt without extra potassium.
In mice eating normal salt, too much potassium (over 1.75% of their diet) makes their blood pressure go up during active hours, especially at high potassium levels like 5%, because of increased activity of certain kidney channels.
Eating more potassium-rich foods doesn't change how much salt is passed in urine or body weight for people with high blood pressure over a year.
For people with high blood pressure, eating more potassium-rich foods leads to higher potassium levels in their bodies after a year, as measured by food records and urine tests.
Causal
People with controlled high blood pressure who ate more potassium-rich foods experienced fewer side effects or discomfort after a year compared to those who kept their usual diet.
People with controlled high blood pressure who ate more potassium-rich foods were more likely to manage their condition with less than half their original medication dose after a year—81% compared to 29% in those who didn't change their diet.
For people with controlled high blood pressure, eating more potassium-rich foods lets them take much less blood pressure medicine after a year—only a quarter of what they started with, compared to 60% for those who didn't change their diet.
In female rats with high blood pressure, antioxidant drugs usually don't lower their blood pressure.
When given a drug called acetazolamide, Tempol lowers blood pressure in older female rats with high blood pressure.
Giving a common antioxidant drug called Tempol to older female rats with high blood pressure did not lower their blood pressure, whether they ate a low-salt or high-salt diet.
After eating a high-salt diet for several weeks, older female rats with high blood pressure had similar blood pressure levels as those on a low-salt diet, around 178 mm Hg in both groups.
In older female rats with high blood pressure, starting blood pressure was similar whether they ate a normal low-salt diet or a high-salt diet, with numbers around 174 and 168 mm Hg.
Exercise made a metabolic regulator in blood vessels 60% more active in obese mice compared to mice that didn't exercise.
Quantitative
Exercise boosted a key signaling protein in blood vessels by 37% in obese mice, which helps improve blood flow.
Exercise increased the activity of a protein that helps blood vessels relax by more than double in the blood vessels of obese mice compared to sedentary mice.
Exercise made a key metabolic regulator in the fat around blood vessels 2.45 times more active in obese mice compared to sedentary mice.
Exercise boosted levels of a protective anti-inflammatory protein in the blood vessels of obese mice by nearly five times compared to mice that didn't exercise.